Alison Ford Workbook by Meeka

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Let’s start by what’s going on inside each and every one of our trillions of cells at all ?mes of the day and night!

Introduction to Cells ( 2.55)

Biochemistry 101

The human body consists of elements and compounds ingested, digested, absorbed, and circulated through the bloodstream to feed the cells of your body.

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The Human Cell

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Introductions

The Human Cell

The cell is the basic structural, func?onal and biological unit of all known living organisms.

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Housekeeping

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Nucleus

contains the cell’s hereditary informa?on

a membrane bound structure

controls the cell’s growth & reproduc?on

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Cytoplasm

Ribosomes

Ribosomes link amino acids togetherprotein synthesis

The cytoplasm consists of all of the contents outside of the nucleus and enclosed within the cell membrane. www .thei ntegr ated healt 9 haca dem y.co m.au

Mitochondria

Cell Membrane The cell membrane is selec?vely permeable to ions and organic molecules controls movement of substances in and out.

Mitochondria are the cell's power producers the baPery of the cell www .thei ntegr ated healt 11 haca dem y.co m.au

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Within cells there is an intricate network of organelles  unique func?ons.

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Cell Structure

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6 12

2 + ATP

Essen?ally, sugar (C6 H12 O6) is burned, or oxidized down to CO2 and H2O, releasing energy (ATP).

All cellular work requires energy ATP or related molecules

O2 is required for this process

Krebs Cycle

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Why do Cells need ATP?

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Cellular respira?on is the process of oxidizing food molecules, like glucose, to carbon dioxide and water. C H O + 6O + 6H O è 12H O + 6 CO

Cellular Respiration

Krebs Cycle (2.00)

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Cellular Respiration

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Take in an adequate supply of water, O2, glucose, amino acids, lipids, vitamins, minerals, to stay alive...

Repair itself. Divide and replace older cells when they are damaged or die.

Carry out the speciﬁc func?on it was designed for.

Respond appropriately to the messages sent to it from other parts of the body.

Powering the Cell – Mitochondria (1.49)

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Biological Functions All biological func?ons are made up of organic molecules

Lipids (fats)

Proteins (amino acids)

Carbohydrates (sugars)

Nucleic Acids

These molecules combine with each other to form more complex molecules e.g. a carbohydrate combines with a protein  glycoprotein

a lipid combines with a protein  lipoprotein

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Biological Functions

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Burn some nutrients and store others for energy...

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Dispose of waste products ...

More Functions of the Human Cell

Enzymes

speed up or catalyse many biological reac?ons

do all of the work inside any cell

allow cells to carry out chemical reac?ons very quickly

facilitate the cell to build things or take things apart

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Function of the Human Cell

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carbohydrates (including ﬁbre), fats, protein and water

needed in smaller amounts

minerals and vitamins

Fat Protein Water

Micronutrients

Vitamins Minerals

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Carbohydrates Chemical chains of sugars

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needed in rela?vely large amounts

Micronutrients

Carbohydrate

Macronutrients Needed in larger amounts

Carbohydrates C,O & H

the most abundant of the macronutrients

are usually in propor?on to form water

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Macronutrients

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Nutrients

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provide > 60% of the energy required by the body easy source of energy needed for: CNS; kidneys; brain; muscles stored in the muscles and liver important for intes?nal health important for waste elimina?on

simple carbohydrates  one or two sugars complex carbohydrates  three or more sugars

Simple Carbohydrates monosaccharides or disaccharides oﬀer very liPle nutri?onal value digested more quickly cause rapid insulin response

Sources of Simple CHO table sugar

corn syrup

honey

molasses

jams

jellies

fruit drinks

sog drinks

lollies

fruit

biscuits

donuts

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Monosaccharides Glucose Galactose (found in milk products) Fructose (found in fruits)

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Simple and Complex CHO’s

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Carbohydrate Facts

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present in our environment in only small quan??es

found mainly in dairy products in the form of lactose

slightly less sweet than glucose

Fructose

found primarily in ripe fruits

usually found with glucose and some?mes sucrose

tastes 60% sweeter than glucose or galactose

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Disaccharides Sucrose Maltose Lactose (glucose + galactose)

(glucose + glucose)

(glucose + fructose)

When you eat one teaspoon of sucrose, your body ‘sees’ 2.5 g of glucose and 2.5 g of fructose.

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Disaccharides

Complex CHO’s contain three or more sugars mostly rich in ﬁbre take longer to digest

Honey is a disaccharide but also contains some vitamins and minerals.

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Glucose is by far the most abundant of the simple sugars.

Galactose

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Glucose

don’t raise the blood sugar levels as much as simple sugars

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don’t cause rapid, high insulin response 41

beans

zucchini

len?ls

whole grains

other leguminous plants and vegetables

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broccoli

Fibre A carbohydrate mainly needed to keep your diges?ve system healthy.

Fibre

the indiges?ble por?on of food derived from plants

changes the nature of the contents of the GI tract by changing how other nutrients and chemicals are absorbed

stabilises glucose and cholesterol levels

Types of Fibre insoluble ﬁbre

Insoluble ﬁbre passes through your intes?nes largely intact.

soluble ﬁbre

Soluble ﬁbre forms a gel when mixed with liquid.

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spinach

Insoluble Fibre FuncEons:

Beneﬁts:

moves bulk through the intes?nes

promotes regular bowel movement

controls and balances the pH (acidity) in the intes?nes

removes toxic waste through the colon in less ?me maintains an op?mal pH in intes?nes to prevent microbes from producing cancerous substances

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Sources of Complex CHO’s

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fruit skins vegetable skins whole wheat products wheat bran corn bran seeds nuts

FuncEons:

Beneﬁts:

binds with faPy acids

prolongs stomach emptying ?me so sugar is released and absorbed more slowly

lowers total cholesterol and LDL cholesterol reduces risk of heart disease

regulates blood sugar

Food Sources of Soluble Fibre oats / oat bran dried beans and peas nuts barley ﬂaxseed fruits such as oranges and apples vegetables such as carrots

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vegetables

Soluble Fibre

Overall Value of Fibre improves skeletal muscle insulin sensi?vity helps burn energy to prevent fat storage endogenous stress reducer with resultant cor?sol release  decreases appe?te increases metabolic rate

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Food Sources of Insoluble Fibre

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psyllium husk

Chemical chains of faPy acids

Fats Saturated

FATS Trans fats

Unsaturated polyunsaturated monounsaturated

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Fats

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whole milk ice cream cream faPy meats coconut oil palm oil coPon seed oil

Unsaturated Fats An unsaturated fat is a fat or faPy acid in which there is one or more double bond in the faPy acid chain.

A fat molecule is:

monounsaturated

polyunsaturated

if it contains one double bond

if it contains more than one double bond.

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Sources of Mono-‐unsaturated Fat nuts vegetable oils canola oil olive oil sunﬂower oil avocado

saﬄower oil corn oil soybean oil

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Sources of Poly-‐unsaturated Fat

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Saturated fats solid at room temperature.

buPer cheese

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A saturated fat is made from a triglyceride bonded to saturated faPy acids.

Sources of Saturated Fat

Trans Fats

the majority of trans fats are formed when liquid oils are made into solid fats like shortening and hard margarine.

a small amount is found naturally, primarily in some animal-‐based foods

made when hydrogen is added to vegetable oil -‐-‐ a process called hydrogena?on

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Saturated Fats

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cakes

muﬃns

pie crusts

pizza dough

most breads

some margarine

vegetable shortening

pre-‐mixed cake mixes

donuts

french fries

chicken nuggets

hard taco shells

chips, crackers

frozen dinners

insulates your body cushions vital organs can be converted into energy used to build new cells cri?cal for normal brain development cri?cal for nerve func?on required to carry and help absorb fat-‐soluble vitamins

Our fats / lipids are stored in our cell membranes and determine the ﬂuidity and integrity of our cells.

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Why are the Types of Fats we Eat Important?

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Bad fats cause: s?ﬀ briPle skin

s?ﬀ membranes

premature ageing

brain cell death

arthri?s

painful muscles and joints

Vegetable oils don't have the same cooking quali?es as saturated fats.

Polyunsaturated fats have lots of double bonds prone to free radical aPack  rancid fat harmful to health

Saturated fats don’t have double bonds so don't perpetuate free radical cascades in the body inert fats

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Cooking with Fats

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biscuits

Function of Fats

Best Fats for Cooking?

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Sources of Trans Fats

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BUTTER and COCONUT OIL are not harmful to your health, and are bePer for cooking with than Ω6 vegetable oils.

Chronic pain

BriMle dry skin

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Swelling

A triglyceride consists of three molecules of faPy acid combined with a molecule of the alcohol glycerol.

Triglycerides The triglyceride level in your blood is measured for blood levels of fat. When we eat faPy meats, cream, ice-‐ cream, cheese or fried foods, we are consuming largely triglycerides. Triglycerides are also produced from sugar!

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Bio-‐availability of Fats Non EssenEal • can be produced  mono-‐ unsaturated and saturated fats

EssenEal • can’t be produced must come from our diet polyunsaturated fats

Major EFA’s Ω6-‐FA

linoleic

γ-‐linolenic

Ω3-‐FA α-‐linolenic eicosapentaenoic (EPA) docosahexaenoic (DHA)

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Delayed healing

Triglyceride

Transporting Essential Fatty Acids

EFA’s are distributed through the same vehicles which carry cholesterol throughout your body.

Lecithin is added allowing oil and water to mix

Proteins and minerals are also involved as carriers in the transport of EFA’s throughout your body

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What’s wrong with our Fats?

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control inﬂamma?on

provide energy to the cells

involved in the control of cholesterol & hormones regulate

Food Sources of Ω3

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Why are Ω3 fats so Important?

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linseed oil chia oil canola oil soybean oil walnut oil oily ﬁsh kangaroo meat seaweed

brain neuro-‐transmiPers

promote inﬂamma?on crucial role in brain func?on crucial role in normal growth and development help s?mulate skin and hair growth maintain bone health regulate metabolism

Food Sources of Ω6

corn oil sesame oil coPon seed oil soybean oil peanut oil grape seed oil evening primrose saﬄower oil sunﬂower oil vegetables oil animal fats

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Why are Ω6 fats so Important?

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maintain reproduc?ve system

Ω6 to Ω3 ra?o ≈ 17:1

ra?o should be 2:1  4:1

Ω6 breaks down to inﬂammatory arachidonic acid in the cell membrane

animal fats are predominantly Ω6

Ω3 Fats Reduce In_lammation

reduce pain sensi?vity

improve lipid membrane ﬂuidity and ﬂexibility

enhance membrane permeability

improve membrane’s ability to withstand mechanical & oxida?ve stress

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Issues to Consider with EFA Balance

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ALA -‐-‐-‐ the vegetarian source of Ω3 does not convert well to EPA

Prof’s M Sydney-‐Smith and Marc Cohen, RMIT University, Master of Nutri?on Study Guide

ﬁght cancer

Lower Ω 6 / Ω 3 Ratio Lower Ω6

Increase Ω3

fried foods

seeds

faPy foods

nuts

processed foods

fresh ﬁsh

Ω6 fats (Pro-‐inﬂammatory)

Ω3 fats (An?-‐inﬂammatory)

Ω3 Supplementation?

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arteries become inﬂamed

reduces ability to

highly suscep?ble to free radical oxida?on due to their unsaturated bonds

Ω3 fats increase absorp?on of an?oxidants

primary diges?on issueshypochlorhydria liver disease obstruc?on of bile ducts insuﬃcient bile salt produc?on deﬁcient pancrea?c enzymes Coeliac disease

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Causes of Fat Malabsorption

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reduces ability to ﬁght infec?ons

increases risk of atherosclerosis

It’s all in the Balance!

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immune system inﬂamed

consider quality and dosage of supplementa?on

Prof’s M Sydney-‐Smith and Marc Cohen, RMIT University, Master of Nutri?on Study Guide

Eicosanoids

Eicosanoids are derived from either Ω3 or Ω6 faPy acids. Ω6

Ω3

pro-‐inﬂammatory

an?-‐inﬂammatory

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Ω6 Fats Promote In_lammation

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parasi?c infec?on 83 Prof’s M Sydney-‐Smith and Marc Cohen, RMIT University, Master of Nutri?on Study guide

Eicosanoids are: ‘super hormones’ because they aﬀect the synthesis of virtually every other hormone in the body the body’s cellular check and balance system

Eicosanoids Ω3 / Ω6 will aﬀect your body’s eicosanoid-‐controlled func?ons

CV disease

triglycerides

joints

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What are Eicosanoids?

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controlled by dietary fat and insulin

Ibuprofen

adrenal cor?costeroids

average Western diet

should be Ω6 : Ω3

Ω6 : Ω3 ≈ 17:1

≈2:1  4:1

Ω6 fats break down to the inﬂammatory arachidonic acid in the cell membrane

membranes become weak, briPle and inﬂamed

Linoleic Acid

Gamma Linolenic Acid (GLA) Dihomogamma Linolenic Acid (DGLA)

Arachidonic Acid

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Aspirin

What’s wrong with our Fats?

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aﬀect eicosanoid produc?on

Alpha-‐ Linolenic Acid (ALA) Stearidonic Acid Ecosatetraenoic Acid Zinc, Vit C, Vit B3 Ecosapantaenoic Acid (EPA) Docosahexaenoic Acid (DHA)

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Non Steroidal Anti-‐in_lammatory Drugs (NSAID’s)

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Conversion is further reduced by 40-‐50% by a high Ω6 in the diet.

Importance of Proteins

among the most important structures in the body

form and shape almost the en?re body

carry out metabolic func?ons

act like master switches

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Protein Chemical chains of amino acids

Formation of Proteins Our DNA codes our proteins produced as a string of amino acids.

They need to achieve a three dimensional shape to carry out their tasks:

regula?ng the body’s processes

3 Dimensional Shape

Proteins gain their shape through a special folding technique.

Each protein achieves a dis?nc?ve shape which helps determine its unique func?on.

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guarding against infec?on

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ALA is converted to EPA along the same pathway as linoleic acid (LA).

LA is the most common Ω6 faPy acid in our Western diet.

The conversion of ALA to EPA in the presence of a high saturated fat diet is limited to 6% and conversion to DHA is 3.8%.

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Problems with ALA Conversion

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Bene_its of Protein involved in cellular energy supports healthy metabolism stabilises blood sugar increases sa?ety maintains a healthy immune system sustains lean muscle

assists hormone produc?on

ability to exercise

Enzymes Needed for Protein Digestion proteinases

proteases

proteins are broken apart by hydrolysis

Messengers Hormones / NeurotransmiPers

The amino acid tyrosine is the precursor to thyroid hormones and dopamine.

The amino acid tryptophan is the precursor to serotonin and melatonin.

ﬂuid balance

messengers

structural elements

buﬀers

transporters

immuno protectors

Enzymes

Metalloproteins  combine with zinc

Flavoproteins  combine with Vitamin B2

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Structural Elements ContracEle proteins cardiac

skeletal muscle

smooth muscle

Fibrous proteins collagen

elas?n

kera?n in bone, teeth, skin, tendons, car?lage, blood vessels, hair and nails

Globular proteins myoglobulin

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A deﬁciency in protein or lean muscle 

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bulk and strength

enzymes

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muscle energy

Roles of Proteins

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premature ageing

Protein is Necessary

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repair post injury

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many enzymes

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Immunoglobulins (Ig) bind to an?gens and deac?vate them

Haemoglobin  O2

Albumin  calcium, zinc, Vitamin B6

Prealbumin  Vitamin A

Transferrin  iron

Ceriloplasmin  copper

Lipoproteins  lipids

Buffers

Proteins regulate the acid/alkaline balance by releasing or accep?ng H+ ions

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Fluid Balance

Proteins such as albumin, aPract water into the blood so low levels can cause leakage of ﬂuids into the inters??al spaces

oedema

Protein diges?on occurs in:

stomach small intes?ne

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Protein Digestion and Absorption

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•  cytokines •  T-‐helper cells (CD4) •  macrophages •  neutrophils

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complement proteins (IgE, IgG, IgA) an?bodies

Transporter Proteins in blood include:

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The Stomach

HCL is produced in the parietal cells in the stomach lining s?mulated by the hormone gastrin

acid chyme passes to the duodenum diges?on occurs with enzymes in the small intes?ne

travels to the liver via the portal vein

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Immuno Protectors

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temperature of the food

acidity of food acidity of stomach

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Gastrin

> 40 yrs old our level of stomach HCL begins to decline

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amount of protein in food

?me

CHO inhibits produc?on of the hormone gastrin which s?mulates the produc?on of stomach HCL

How do PPI’s Work? They bind to the ATP’ase proton pump at the secretary surface of the parietal cell, therefore inhibi?ng Hydrogen release into the gastric juice.

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113

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PPI’s (Proton Pump Inhibitors)

medicines which work by reducing the amount of stomach acid made by glands in the lining of the stomach

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enzymes concentra?on

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presence of diges?on inhibitors (antacids)

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Determinants of Protein Digestion in the Stomach

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Somac

Omneprazole

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Losec

Damaging effect of PPI’s shut down produc?on of HCL acid therefore the ability to absorb protein

zinc

magnesium

iron

calcium

Vitamin B12

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Protein in the Small Intestine Protein diges?on con?nues in the upper por?on of the small intes?ne under the ac?on of the pancrea?c protein enzymes:

trypsin

chymotrypsin

Protein in the Small Intestine The amino acids are absorbed by the blood capillaries of the small intes?nes

carried through the liver

general circula?on.

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Nexium

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Protein Synthesis & Degradation

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Proton Pump Inhibitors (PPI’s)

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protein breakdown

40% of all protein in the body is in muscle

muscle accounts for approx 25-‐35% of all protein turnover

rates of protein synthesis (anabolic) and degrada?on (catabolic) are under independent control

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Protein Synthesis & Degradation maintenance of lean muscle mass is aﬀected by:

the ability to synthesize protein

and its breakdown

Protein Synthesis Requirements

cofactors Zinc and Vitamin B6

adequate intake of protein and a full range of amino acids

vegetarian protein sources are variable in amino acid content

adequate stomach acid for primary diges?on

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Protein Synthesis & Degradation

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protein synthesis

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Amino Acid Degradation

Insulin and growth hormone are anabolic.

Cor?sol and glucagon are catabolic as are cor?costeroids eg. Prednisone.

The carbon skeletons of the amino acids are used to produce glucose.

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glucagon

some amino acids are broken down to form glucose

others produce ketone bodies when blood sugar is low

Amino Acid Degradation In ?mes of excess ⏎ea?ng high energy foods

protein is turned into faPy acids in adipose ?ssue = FAT

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Amino Acid Degradation

Amino acid carbon skeletons can be used to produce: energy

glucose

ketone bodies

cholesterol

faPy acids

Protein breakdown gives oﬀ ammonia

used in urea synthesis

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Protein Breakdown  Urea

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cor?sol

to s?mulate the breakdown of amino acids in the liver to form glucose and restore blood levels  gluconeogenesis

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Too much insulin with blood glucose swings promotes higher levels of:

Amino Acid Degradation

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Protein Breakdown Urea Low serum urea < 5.0 indicates low protein breakdown and a probable protein deﬁcient state

High serum urea may indicate excess protein catabolism. (possibly high levels of cor?sol in the blood from stress)

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Gluconeogenesis

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cysteine

glycine

glutamate

Glutathione (GSH) Depletion

GSH is depleted with protein deﬁciency  inﬂamma?on and disease

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Creatine Crea?ne is part of crea?ne phosphate stored in muscle for rapid ATP produc?on and energy requires amino acids:

arginine

glycine

methionine

Carni?ne is required for transport of long chain faPy acids across the inner mitochondrial membrane for oxida?on and energy in the cell  requires amino acids:

lysine

methionine

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Carnitine

137

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The body’s most powerful an?oxidant glutathione (GSH) requires amino acids:

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Urea is mostly excreted in the urine but 25% is secreted onto the intes?nal lumen where bacteria turn it back to ammonia  upset bowel.

Amino Acids – Important building blocks

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Daily Protein Requirement Protein requirement (g) •  = ideal weight (kg) x 0.9 x Exercise Factor (EF) 1

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Protein Breakdown  Urea

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Exercise level is high

Mul?system Ques?onnaire (MSQ) score is 7 or above.

Low = exercise < twice a week = EF1.2

Medium = low intensity exercise 3-‐6 ?mes a week = EF 1.3

High = medium-‐high intensity exercise 3-‐6 ?mes a week = EF 1.5

MSQ Scoring In good health, the score for any one category should be:

< 10% of the total possible for that category

and the total score should be < 15.

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What is Lean Body Mass?

Lean Body Mass is comprised of everything in your body except body fat.

For the average adult male ≈ 42% of body weight is skeletal muscle and ≈35% for females.

LBM is a component of body composi?on, calculated by subtrac?ng body fat weight from total body weight:

Total Body Weight

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Calculation of Lean Body Mass (LBM)

= lean + fat + bone etc. 143

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BMI is < 19.5

No exercise = EF 1.1

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Mul?ply by an EF of 1.2 if:

Exercise Levels Graded as:

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Mathematical Formula (LBM) men: LBM = (0.32810 * W) + (0.33929 * H) -‐ 29.5336

women: LBM =( 0.29569 * W) + (0.41813 * H) -‐ 43.2933 *W is body weight in kilograms *H is body height in cen?metres

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Calculating Daily Protein Requirement

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De_icient Protein Intake Deﬁcient protein intake, primary diges?on, absorp?on or synthesis, par?cularly in conjunc?on with excess catabolism, will cause:

general fa?gue

muscle fa?gue

endurance

recovery post injury

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How much Protein? Group

Protein Intake (g/kg/day)

Sedentary men & women

0.8-‐1.0

Moderate-‐intensity endurance athletes (a)

1.2

Recrea?onal endurance athletes (b)

0.8-‐1.0

Football, power sports

1.4-‐1.7

Resistance/Endurance (early training)

1.5-‐1.7 (male) 1.3 – 1.5 (female)

Resistance/Endurance (steady state)

1.0-‐1.2 (male) 1.0 (female)

Note: Calculate protein at your healthy body weight (a) Exercising approximately four to ﬁve ?mes per week for 45-‐60 min (b) Exercising four to ﬁve ?mes per week for 30 min at <55% VO2peak

Name

PorEon

Protein (grams)

Beef, lean ﬁllet, grilled

100g

Chicken, breast, grilled

100g

Fish, white ﬁllet, grilled

100g

Tuna, canned

100g

Eggs

2 whole

Milk and soy milk

1 cup (250ml)

Yoghurt, natural

1 cup (200g)

Cheese

40g

10.6

CoPage cheese

½ cup

Legumes

½ cup

Almonds

50g (1/3 cup)

Pea protein isolate powder

25g

Male 53 years old Weight: 78kg

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Good Sources of Protein

Case Study 1 Male 53 years old

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Case 1: Food Diary Breakfast

Protein (grams)

2 eggs with 2 slices sourdough

Mid morning Height: 183cm Healthy weight range: 67-‐84kg

Trail mix (¼ c dried fruit & ¼ c nuts) Medium skim laPe (200ml milk) Lunch

9 10

Mango chicken salad

Ac?vity levels: Sailing x3; gym x 2; stretch rou?ne/hiking bench daily

Mid a[ernoon

1.5 gram protein/kg healthy body weight

4 Vitaweets with vegemite & tomato 3 200ml Sustagen Sport , Vanilla (made on 250ml milk) 24 Dinner

Protein requirements: 1.5 x 78kg = 117g

Teriyaki ﬁsh with vegetables 200g yoghurt with fruit TOTAL:

40 14 148 grams

Case Study 2 Female 40 years old

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Case 2: Food Diary Breakfast Yoghurt Berry Crunch: ¼ c homemade high protein granola, 100g yoghurt, berries Mid morning 30g (¼ c) nuts Lunch Tuna salad with quinoa Mid a[ernoon Smoothie (LSA and 1 x fruit added) Dinner Mediterranean chicken and haloumi salad TOTAL:

Female: 40 years old Weight: 70kg Height: 163cm Healthy weight range: 49-‐66kg Ac?vity levels: 4-‐5 ?mes per week (average 45-‐60 mins) 1.2 gram protein/kg healthy body weight Protein requirements: 1.2 x 66kg = 79.2g

Protein during and after exercise Protein 10g

Muscle and protein metabolism

•  Protein breakdown •  Nega?ve balance

During exercise:

23g 12g

Post exercise: •  Protein recovery •  Posi?ve balance •  24 hour eﬀect

41g 92g

Post exercise snack Protein and carbohydrate combo Carbohydrate -‐> insulin amino acids Protein  muscle uptake eten?on of amino acids Examples: • Natural yoghurt with 1 x fruit; Ryvitas with tuna; 1x banana and 30g almonds; fruit smoothie with protein powder Intense workouts e.g. WPI (Whey Protein Isolate)

Can you eat too much Protein? Yes! > 2g protein/kg body weight Calcium excre?on  weakened bones Progression of kidney disease (if suscep?ble to CKD) Weight gain if you don’t expend the calories! • 1g protein = 4 calories • 1g carbohydrate = 4 calories • Extra calories from either = weight gain!

AIS Website

cell life

chemical and metabolic reac?ons

transport of nutrients

body temperature regula?on

elimina?on of waste

Water -‐-‐-‐ Chemical and Metabolic Reactions Water removes waste products including toxins which the organs’ cells reject, and removes them through urine and faeces.

minerals

vitamins

glucose

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distribu?ng essen?al nutrients to cells

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Water a carrier

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provides ﬁve vital func?ons in your body :

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a major cons?tuent of our bodies and vital organs

Water

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Body Temperature Regulation

limits changes in body temperature

allows the body to release heat

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Water

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This threshold of drinking water enables to balance water losses and keep the body properly hydrated.

✚ Dangerous to Overhydrate Overhydra?on can be serious causing chemical changes in the brain

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Measuring Body Composition

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Morning Tea

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acts as a shock absorber for eyes, brain, spinal cord and even for the foetus through amnio?c ﬂuid

A healthy adult (sedentary) living in a temperate climate should drink 1.5  2 litres of water per day.

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an eﬀec?ve lubricant around joints

How much Water?

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Micronutrients Nutrients required throughout life in small quan??es to facilitate a range of physiological func?ons ...

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Function of Water

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Vitamins & Minerals

Fat Soluble and Water Soluble Vitamins Fat Soluble Vitamins Water Soluble Vitamins

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Fat Soluble Vitamins Fat-‐soluble vitamins are:

•  stored in the fat ?ssues and liver •  easier to store than water-‐ soluble ones •  can stay in the body as reserves for days or months

Fat soluble vitamins do not dissolve in water

•  they can only be absorbed through the small intes?ne in combina?on with fat

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Fat Soluble Vitamins

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13 recognized vitamins

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Organic compounds found naturally in food

Vitamins

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Fat Soluble Vitamins Vitamins A, D, E and K

available in a well balanced diet together with sunlight exposure

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Vitamins

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do not get stored in the body for long  quickly expelled through urine

Vitamin A Fat Soluble immune func?on vision reproduc?on cellular communica?on

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De_iciency of Vitamin A

blindness

increased viral infec?on

Two forms of Vitamin A are available in the human diet: Preformed Vitamin A: •  dairy products •  ﬁsh •  meat

Pro Vitamin A carotenoids (precursors to re?nol) : •  oils •  fruit •  vegetables

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Vitamin A

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need to be replaced more ogen

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Vitamins C and all B Vitamins

The Vitamin Wheel

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Sources of Vitamin A sweet potatoes carrots pumpkin dark leafy greens apricots tuna

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Water Soluble Vitamins

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Vitamin B2  Ribo_lavin essen?al for metabolizing fats and proteins

maintaining healthy: vision

hair

skin

liver

cellular energy

nervous system

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Vitamin B2

Most people obtain adequate Vitamin B2 in a normal diet

however the elderly or people with diges?ve issues may be at risk of deﬁciency.

yeast almonds whole grains mushrooms nuts lean meat green leafy vegetables milk eggs

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Sources of Vitamin B2

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Vitamin B3 Niacin helps make various sex and stress hormones in the adrenal glands and brain neurotransmiPers

aids circula?on

water soluble  cannot be stored by the body beneﬁcial for: high cholesterol

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grains legumes for?ﬁed breads asparagus nuts seeds cabbage broccoli green leafy vegetables

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plays a key role in energy produc?on, and breakdown of carbohydrates and fats

destroyed by heat  depleted in the cooking process

Sources of Vitamin B1

atherosclerosis

diabetes

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Vitamin B1 Thiamine

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beetroot yeast dairy poultry lean meat eggs

Vitamin B4 Adenine helpful in the making code of DNA

essen?al in cellular respira?on

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Sources of Vitamin B3

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ﬁsh

fresh fruits whole grains honey herbs

Vitamin B5 Panthothenic Acid among the most important of the B group vitamins

vital in the breakdown of fats, carbohydrates and proteins

Sources of Vitamin B5 cauliﬂower mushrooms sweet potatoes broccoli

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vegetables

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Vitamin B6 Water soluble vitamin naturally present in many foods.

Mostly concerned with: protein metabolism

cogni?ve development

neurotransmiPer synthesis

gluconeogenesis

Most people with a well balanced diet obtain adequate amounts of Vitamin B6.

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Sources of Vitamin B4

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cereals potatoes bananas

helps with growth and replica?on of cells maintains blood sugar levels assists in the produc?on of faPy acids

Sources of Vitamin B7 milk cheese buPer poultry cauliﬂower bananas watermelon peas

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Vitamin B9  Folate or Folate Acid crucial for brain func?on important role in mental and emo?onal health aids the produc?on of DNA and RNA important when cells and ?ssues are developing rapidly works closely with Vitamin B12 to help make red blood cells

common to have low levels of folic acid  supplements are recommended, especially in pregnancy

pregnant women need more folic acid to lower the risk of neural tube birth defects spina biﬁda

cleg palate

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Vitamin B9 Folic Acid

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tuna chicken

helps restore hair loss and keeps skin and nails healthy

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chickpeas

Vitamin B7Biotin

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Sources of Vitamin B9 spinach dark leafy green vegetables asparagus

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Sources of Vitamin B6

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brain damage 197

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myelin surrounding nerve cells

mental ability

red blood cell forma?on

break down of some faPy acids to produce energy

Pernicious Anaemia In pernicious anaemia  deﬁciency of intrinsic factor, a protein essen?al for subsequent absorp?on of Vitamin B12 in the ileum.

Symptoms include: ?redness

lack of appe?te

weight loss

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depression

200

Vitamin B12 De_iciency Serum B12 levels are not indica?ve of ?ssue levels.

Serum level can be high while the ?ssue level is low. The lower range of ‘normal’ serum B12 is 150pmol/L whereas levels < 400pmol/L have been associated with brain shrinkage and neurological damage.

liver

meat milk cheese eggs mushrooms almost anything of animal origin

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Sources of B12

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help to produce and maintain:

Vitamin B12 deﬁciency is commonly found in the elderly with poor diges?on, and vegans who don’t eat animal products.

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Cyanocobalamin and Methylcobalamin

Vitamin B12

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Neuropathic Pain and B12 Burning neuropathic pain can be caused by a low B12 level.

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Vitamin B12

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a potent an?oxidant

cardiovascular disease

coronary heart disease

stroke

Vitamin C shortens the dura?on of the common cold

deﬁciency can be fatal scurvy

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Sources of Vitamin C oranges grapefruit kiwifruit tomatoes potatoes spinach

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Vitamin C Content of Fruits

Vitamin E

Vitamin E deﬁciency is very common

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essen?al in numerous enzyma?c reac?ons

Higher intakes of Vitamin C are associated with reduced risk of:

most people eat half the recommended dietary allowance

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a water soluble vitamin, therefore humans must obtain from their diet

Vitamin C

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Vitamin C Ascorbic acid

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turnips asparagus almonds

Vitamin K Also necessary for the ac?va?on of a protein called osteocalcin, which is used in the mineralisa?on of bone.

Vitamin K deﬁciency has been linked with arthri?s.

menaquinone (K2), produced in bacteria

Dietary Vitamin K is essen?al in the blood clo•ng process, playing a role in both the development of blood clots and in the preven?on of clo•ng.

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Sources of Vitamin K kale spinach lePuce rocket cabbage

Inorganic substances, which the body needs for vital processes…

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Minerals

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olives spinach

2 types of Vitamin K phylloquinine (K1), found in plant foods only

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avocados

Vitamin K

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Minerals There are two types of minerals:

macrominerals

microminerals

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sunﬂower seeds

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Sources of Vitamin E

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Calcium (Ca) Magnesium (Mg) Phosphorus (P) Potassium (K) Sulfur (S) Chlorine (CI) Sodium (Na)

Microminerals (trace minerals) Iron Cobalt Chromium Copper Iodine Manganese Selenium Zinc Molybdenum

Minerals  Dietary Sources dairy products, green leafy vegetables  CALCIUM nuts, soy beans, cocoa  MAGNESIUM cel?c sea salt, milk, spinach  SODIUM legumes, whole grains, bananas  POTASSIUM

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Macrominerals

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Types of Malnutrition

Malnutri?on is a group of condi?ons generally related to poor quality or insuﬃcient quan?ty of nutrient intake, absorp?on, or u?liza?on.

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red meat, leafy vegetables (especially spinach)  IRON

Protein-‐energy malnutriEon

Micronutrient deﬁciency diseases

resul?ng from deﬁciencies in any or all macronutrients

resul?ng from a deﬁciency of speciﬁc micronutrients

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Types of Malnutrition

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Speci_ic De_iciencies

Vitamin K

Vitamin A

Vitamin D

•  blood clots can’t form and spontaneous bleeding can occur. •  Poor brain and eye health

•  brain will not develop properly •  blindness •  excep?onally vulnerable to infec?ons

•  Schizophrenia •  Alzheimer’s •  Parkinson’s •  Depression •  SADs •  some autoimmune diseases

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Magnesium De_iciency Low serum and intracellular Magnesium is associated with: insulin resistance

impaired glucose tolerance

decreased insulin secre?on

Without magnesium, our pancreas won’t secrete enough insulin or the insulin it secretes won’t be eﬃcient enough to control our blood sugar.

Magnesium in our cells helps the muscles to relax but if we can’t store magnesium because the cells are resistant, we lose magnesium.

blood vessels constrict

aﬀects our energy levels

increases blood pressure

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Magnesium  Insulin Ef_iciency

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can be due to a number of causes including dietary deﬁciency, or condi?ons which interfere with the u?liza?on of a nutrients

Protein Energy Malnutrition

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in?mate connec?on between diabetes and heart disease

closed loop between declining magnesium levels

declining insulin eﬃciency

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Micronutrient De_iciencies

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Type 2 Nutrients •  nitrogen, sulphur, essen?al amino acids, potassium, sodium, magnesium, phosphorous, zinc, water

Ascorbic Acid

Iron

Calcium

Thiamine

Re?nol

Tocopherol (Vitamin E)

Vitamin D

(Vitamin A)

Nico?nic Acid

Cobalamin

PyridoxineIodi ne

Copper

Manganese

Riboﬂavin

Vitamin K

Folate

Type 1 Nutrient De_iciencies

Anaemia

Beri Beri

Pellagra

Scurvy

Xeropthalmia

Rickets

•  Iron

•  Thiamine

•  Niacin

•  Vitamin C

•  Vitamin A

•  Vitamin D

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Type 2 Nutrients nitrogen

sulphur

essen?al amino acids

potassium

sodium

magnesium

zinc

phosphorus

A deﬁciency of any one of the Type 2 nutrients can cause the body to eliminate the others in order to keep them in balance.

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The Body will Triage to stay Alive

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Micronutrient Triage

DNA damage and late onset disease can be consequences of a triage alloca?on of response to micronutrient scarcity.

For example, if you have a zinc deﬁciency, the body will excrete magnesium in the urine, despite a rela?ve magnesium deﬁciency. 233

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•  all vitamins, most trace elements, calcium

Selenium

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Type 1 Nutrients

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Type 1 and Type 2 Nutrients

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Vitamin B Deﬁciency, Bowel Dysbiosis

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Liver or Gall Bladder Problem

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Vitamin B6 Deﬁciency

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Manifestations of Nutrient De_iciencies

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Vitamin B2 Deﬁciency

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Lack of zinc, iron, protein, and calcium Vitamin B7 Deﬁciency

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Vitamin B Deﬁciency, Protein Deﬁciency (evidence of previous ill health)

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Vitamin A Deficiency, Calcium Deficiency, EFA Deficiency

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Zinc Deﬁciency, Vitamin B6 Deﬁciency

Deﬁciencies in: Calcium Magnesium Zinc Sulfur

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Vitamin C Deﬁciency, Calcium Deﬁciency

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Vitamin K Deﬁciency, Kidney Disease

Iron, Vitamin B2, possibly other B Vitamins

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Deﬁciencies in: Vitamin A EFA

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Vitamin B2 and Vitamin B6 Deﬁciencies

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Deﬁciencies in: Zinc, Vitamin B6, Sulfur, Selenium, Bio?n, -‐-‐-‐ ? IBS

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Deﬁciencies in: Vitamin B12, Folate, other B vitamins, Iron

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Vitamin B2 Deﬁciency

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Vitamin B2, Vitamin B6, Zinc Deﬁciencies

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Thyroid Deﬁciency

Protein Deﬁciency

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Essen?al FaPy Acids

Observational Practice Signs of Nutrient Deﬁciencies

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? The Big Questions

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What is inﬂamma?on? Why is it a problem?

as a driver of chronic pain and illness...

In_lammation Our body’s natural response to injury is to create swelling and pain is an inﬂammatory response.

Acute In_lammation (3:46)

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Morning Tea

In_lammation

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Lunch

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In_lammation is Vital to our Survival Inﬂamma?on is not always a nega?ve reac?on.

It is also usually an indica?on that the body is trying to defend itself against something it perceives as poten?ally harmful.

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Problems arise when inﬂamma?on gets out of control

It’s not supposed to be turned on for prolonged periods of ?me and never forever.

Cellular Destruction It spreads to every part of the body through the blood stream.

This leads to a reduc?on of cellular func?on followed by cellular destruc?on.

When inﬂamma?on goes awry, a variety of chemicals are produced  toxic to our cells.

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The Problem wit In_lammation

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What Causes In_lammation? Trauma/accident Insulin Resistance Essen?al faPy acid imbalance Gut disturbance Food allergies/intolerance Toxic overloadpoor liver detoxiﬁca?on Exposure to environmental toxins/ metals Oxida?ve stress Insomnia-‐ disturbed body biorhythm

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Premature Ageing Obesity Osteoarthri?s Fibromyalgia Chronic pain Asthma Alzheimer’s Disease Cancer Diabetes Cardiovascular Disease Heart Disease Rheumatoid Arthri?s Ankylosing Sponylosis Autoimmune Disease Osteoporosis Allergies Depression

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In_lammatory Cytokines serve as molecular messengers between cells

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What are examples of In_lammatory Diseases?

products of immune cells  act as mediators and regulators of immune processes

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Chronic In_lammation (1:34)

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Chronic Stress or chronic infec?on 269

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used clinically as biological response modiﬁers for the treatment of various disorders

Types of Cytokines Monokines cytokines produced by mononuclear phagocy?c cells

Lymphokines cytokines produced by ac?vated lymphocytes, especially Th cells

Interleukins

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In_lammatory Cytokines

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cytokines which act as mediators between leukocytes

Progressive ?ssue damage secondary to low an?oxidant status

Are Sugars Evil? Blood sugar needs to be kept rela?vely constant.

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High levels are toxic to the body. Ager a high carbohydrate meal or snack, the brain s?mulates the pancreas to secrete insulin to deposit glucose into the cells as fat. 275

Insulin Resistance

A driver of inﬂamma?on

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Excessive pro-‐inﬂammatory Eicosanoid synthesis related to EFA imbalance

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In_lammation Physiology

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Carbohydrates which break down quickly during diges?on have a HIGH GI.

LOW GI foods release glucose gradually into the bloodstream.

(>70)

HIGH GI foods release their glucose into the blood quickly.

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Glycaemic Index

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They are compared with white bread as a reference food, which is given a GI score of 100.

The GI compares foods which have the same amount of carbohydrate, gram for gram.

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Carbohydrate-‐ containing foods can be rated on a scale called the Glycaemic Index (GI).

This scale ranks foods based on their eﬀect on blood sugar levels over a period of ?me.

Glycemic Index

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Glycemic Index

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Carbohydrate content of a standard apple = 15 GL= (GI x Carbohydrate content) ÷ 100 = (40 x 15) ÷ 100 = 6

types of sugar rate of absorp?on and diges?on of food

serving size

prepara?on

fat, CHO, ﬁbre content

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What In_luences GL?

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The Dangers of a High Carb Diet Perpetual high carb diets put too much stress on insulin  more insulin is needed to have the same eﬀect. Insulin resistance  the development of a reduced sensi?vity to insulin over ?me

Promotes inﬂamma?on, diabetes, pain and cancer

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Pancreatic function (3.06)

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GI of a standard apple = 40

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A food's GL is determined by mul?plying its GI by the amount of carbohydrate the food contains in each serve and dividing by 100.

Glycemic Load (GL) is a measure of both the quality (the GI value) and quan?ty (grams per serve) of a CHO in a meal.

Calculating GL

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Insulin and role Anabolic hormone involved in glucose, lipid and amino acid/protein synthesis and storage S?mulates the uptake of excess blood glucose by muscle and adipose ?ssue

Inhibits synthesis of glucose by the liver (gluconeogenesis)

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Glycaemic Load (GL)

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•  oxida?ve stress •  increased levels of reac?ve oxygen

Disturbed cell vibra?onal frequency aﬀects eﬃciency of insulin receptors. (Haber, 2003)

Insulin acts on receptors in the cell wall to allow glucose into the cell.

The receptors ﬂoat in a ﬂuid layer around the cell and the vibra?onal frequency of the receptor to the cell must match. Reed G, 2008, ‘Nutri?on in Insulin Resistance & Type 2 Diabetes’, Lecture notes, Residen?al School, Australian College of Holis?c Medicine

Insulin Sensitivity to the Cell A diet with excess CHO’s but nutrient deﬁcient

•  precursor to insulin resistance and further inﬂamma?on

Reed G, 2008, ‘Nutri?on in Insulin Resistance & Type 2 Diabetes’, Lecture notes, Residen?al School, Australian College of Holis?c Medicine

Essential Co-‐factors Zinc and chromium aPach to the receptor and allow it to spin more easily and balanced

EFA’s inﬂuence the ﬂuidity of the cell wall

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Insulin Sensitivity to the Cell

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Reed G, 2008, ‘Nutri?on in Insulin Resistance & Type 2 Diabetes’, Lecture notes, Residen?al School, Australian College of Holis?c Medicine

Lifestyle Factors affecting Insulin Resistance

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High glucose levels are associated with:

Nutrient deﬁciencies in the diet aﬀect insulin sensi?vity.

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Causes of Insulin Resistance

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Insulin in Your Body (3.40)

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The Pill increases Insulin Resistance by 27%

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Clausen, J Clin Invest, 1996

pro-‐inﬂammatory cytokine secre?on

immune cell inﬁltra?on

disrupted func?on of ?ssues involved in glucose homeostasis

Waist Measurement

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Obesity linked to Chronic In_lammation Pro-‐inflammatory cytokine tumour necrosis factor (TNF) expressed in adipose ?ssue of obese mice and linked to insulin resistance Circula?ng free faPy acids (FFAs) have a nega?ve effect on insulin target ?ssues through the ac?va?on of inflammatory pathways and impaired insulin signaling

The adipocytes in fat stores act as an endocrine organ, releasing bioac?ve substances, adipokines: • interleukin(IL)-‐6,IL-‐1b •  TNF-‐a •  lep?n • adiponec?n McArdle et al, 2013 ‘Mechanisms of obesity-‐induced inﬂamma?on and insulin resistance: insights into the emerging role of nutri?onal strategies’ Nutrigenomics Research Group, UCD Conway Ins?tute, School of Public Health, Physiotherapy and Popula?on Science, University College Dublin, Dublin, Republic of Ireland

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Obesity drives Insulin Resistance and In_lammation

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Obesity linked to Chronic In_lammation

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Obesity

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Obesity drives Insulin Resistance and In_lammation As obesity progresses, adipose ?ssue macrophage phenotype switches from an?-‐ inﬂammatory M2 to the pro-‐inﬂammatory M1 type.

M1 adipose ?ssue macrophage inﬁltra?on decreases insulin sensi?vity as a result of greater TNF-‐a, IL-‐1b, and IL-‐6 secre?on.

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Pro-‐inﬂammatory TH1 cells secrete IFN-‐g  drives polariza?on of pro-‐inﬂammatory macrophages secrete IL-‐1,IL-‐6,andTNF-‐a

Insulin should peak within 30  60 mins and should not exceed 60 mU/L.

Post prandial glucose is lower than at the start of the test indica?ng hypoglycaemia

Glucose mmol/L

Glucose

Insulin

14 12 10 8 6 4 2 0

Time 2

Insulin Resistance with Hyperinsulinaemia ~BUT~ normal glycaemic curve and latephase hypoglycaemia

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Glucose Tolerance Test:

100 90 80 70 60 50 40 30 20 10 0

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Insulin mU/L

Hypoglycemia

Hypoglycaemia < 4 mmol/L.

Some people may feel symptoms when their level is > 4 mmol/L .

Hypoglycaemia requires increased cor?sol to s?mulate breakdown of muscle glycogen stores and glyconeogenesis in the liver to restore blood glucose levels.

Increased cor?sol produced by the metabolic stress of swinging blood sugar promotes catabolism of muscle and deposi?on of central fat.

Wilson, J, 2010, Adrenal Fa?gue; “The Big Burn Out” A5M, 4th Annual Conference in An?-‐Aging Medicine & Aesthe?c medicine

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Hypoglycaemia

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T Helper 1 cell numbers increase with obesity.

Dendri?c cells secrete cytokines in response to extracellular signals from adiponec?n and FFA’sini?ate a T cell response.

Glucose Tolerance Test

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Hypoglycaemia Chronically increased cor?sol related to hypoglycaemia leads to:

hyperlipidaemia

central obesity

increased risk of atherosclerosis

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Obesity drives Insulin Resistance and In_lammation

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increases fat deposi?on

shakiness before meals or when hungry

addic?on to CHO-‐rich foods

insomnia relieved by ‘midnight snacks’

frequent mood swings

episodic irrita?on or aggression

The Merck manual of diagnosis and therapy, 17th Ed, Sec?on 220

Nutrients to Reduce Hypoglycemia •  Improvement in symptoms: •  57% of magnesium-‐ treated subjects

Magnesium

•  Chromium might help keep blood sugar levels normal by improving the way the body uses insulin.

•  100 mg per kg per day of the Vitamin B3 alleviates Hypoglycaemia.

Chromium

Vitamin B3

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Preventing Reactive Hypoglycaemia frequent snacks avoidance of reﬁned carbohydrates protein-‐rich diet high complex CHO diet supplements: • chromium picolinate • magnesium chelate • B complex

Diabetes is a disturbance of fat metabolism as much as a disorder of sugar metabolism.

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stress reduc?on

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Type 2 Diabetes

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breakdown of muscle glycogen stores

sleepiness ager meals

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blocks insulin signalling

Symptoms of Reactive Hypoglycaemia

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Type 2 Diabetes -‐-‐-‐ Multiple Pathology hyperlipidaemia elevated uric acid chronic inﬂammatory disease hypertension cardiovascular complica?ons re?nal damage peripheral neuropathy faPy inﬁltra?on of the liver

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High Levels of Cortisol

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weight loss vaginal candidiasis The Merck Manual, 17th Ed, Sec?on 2

A Question? Could intes?nal dysbiosus be a contribu?ng factor for sugar cravings, a pre-‐diabe?c state and eventual diabetes?

unexplained decline in energy levels and vitality recurrent intes?nal and/or vaginal candidasis

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Genetic Factors Mul?ple genes are involved: polymorphisms are speciﬁc to localised ethnic popula?ons including the Australian Aborigine

Complex interplay between genes which regulate: insulin sensi?vity

lipid metabolism

hormonal regula?on

Carbohydrate Responsive Element Binding Protein (ChREBP) is an important diet-‐responsive polymorphic gene:

a pivotal transcrip?on factor which: shigs glucose metabolism into fat synthesis

inhibits faPy acid oxida?on

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Genetic Factors

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polydipsia excessive (abnormal thirst)

cogni?ve decline

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polyuria (excess urina?on)

Other Symptoms excessive mood swings and/or

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Genetic Factors

ChREBP expression  with high dietary CHO intake

with high PUFA intake

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symptoma?c hyperglycaemia

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Symptoms Onset of Type 2 Diabetes

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Type 2 diabetes

obesity

normal glucose tolerance (25% of non-‐ obese individuals)

Type 1 Diabetes

implementa?on of dietary and lifestyle programs to help prevent the progression

Risk Factors for Chronic Diseases

Metabolic Syndrome Syndrome X Includes: abdominal obesity high blood pressure low blood levels of 'good' cholesterol, HDL high blood levels of the 'bad' cholesterol, LDL high blood levels of triglycerides

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Metabolic Syndrome (1.05)

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Metabolic Syndrome

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impaired glucose tolerance

early detec?on is vital

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people with:

Early Detection  Lifestyle Changes

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Metabolic Syndrome or Syndrome X Metabolic Syndrome is not a disease in itself, but a collec?on of risk factors which ogen occur together.

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Who has Insulin Resistance?

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insulin resistance

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insulin resistance

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abdominal obesity

high BP

high blood levels of

triglycerides

low blood levels of HDL

high blood levels LDL

Mitigating the Risk

Diet and Lifestyle changes

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Cardiovascular Disease dysfunc?onal condi?ons of: heart

arteries

veins

If O doesn’t arrive, the ?ssue or organ will die. 2

Ischaemic Heart Disease

Excess build up of fat or plaque are respec?vely termed arteriosclerosis and atherosclerosis.

Ischaemic Heart Disease results because excess fat or plaque deposits are narrowing the veins which supply oxygenated blood to the heart.

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Stress Cortisol and Muscle Catabolism

Stress drives cor?sol levels up and creates a rela?ve DHEA deﬁciency.

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Cor?sol is catabolic and breaks down muscle to mobilise amino acids to be converted to glucose by the liver.

High cor?sol promotes deposi?on of central fat.

Wilson, J, 2010, Adrenal Fa?gue; “The Big Burn Out” A5M, 4th Annual Conference in An?-‐ Aging Medicine & Aesthe?c medicine, Pre-‐Conference Clinical Workshop

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age

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Signs of Metabolic Syndrome

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hypoglycaemia insulin resistance

emo?ons

pain

lack of sleep

Further Dangers of a High CHO Diet Excessive mood swings and/or cogni?ve decline

Unexplained decline in energy levels and vitality; sleep disturbances

Implica?ons for healing post-‐injury?

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Drivers of Stress Cortisol

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stressful situa?ons

Without stomach acid you can’t absorb protein, magnesium, calcium, zinc, iron and Vitamin B12.

Hidden Sugars

Sugars, Obesity and Arthritis A 2012 University of NSW popula?on health study has linked the consump?on of sugary drinks to a rapid increase in obesity in Australia.

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Afternoon Tea

26g Sugar = 5 tsp 335

One can of sog drink contains on average 16 teaspoons of sugar.

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A diet high in sugars inhibits the produc?on of stomach acid.

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Further Dangers of a High CHO Diet

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?ssue damage

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inﬂamma?on

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Fructose in Food Sweet foods contain large quan??es of added fructose, ogen in the form of High Fructose Corn Syrup (HFCS) desserts

cakes

biscuits

chocolate

lollies

fruit drinks

cordials

sog drinks

Much of our fructose is derived from sucrose.

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Glucoreceptors (GLUTS)

Body cells cannot just help themselves to blood sugars. They need to have a special protein within the cell to absorb the sugar and then use it in a chemical process.

A GLUT exposes an indent on the outside of a cell into which only one type of molecule will ﬁt. The GLUT then pushes the sugar through the cell wall and waits for the next molecule.

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Glucoreceptors (GLUTS)

Sucrose = 50% fructose + 50% glucose.

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Fructose is a monosaccharide, which the body can use for energy.

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Fructose occurs naturally in fruits, vegetables and honey.

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Fructose

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GLUTs

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GLUT 3

GLUT 4

GLUT 5

‘keep every

glucose and fructose

glucose only

fructose only

cell alive’ protein (glucose only)

responsible for the low-‐level of basal glucose uptake for cell respira?on

Levels are: •  increased by reduced glucose levels •  decreased by increased glucose levels

a major receptor for uptake of Vitamin C as well as glucose

GLUT 2  Fructose

Fructose is absorbed through the GLUT 2 proteins but they are pushed straight back out again no insulin is produced.

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GLUT 3  for Thinking

not dependent on the presence of insulin

a specialist transporter located predominantly in the brain

keeps vacuuming glucose out of the blood

present in large numbers in muscle and fat ?ssues

how insulin s?mulates energy use by muscles and fat storage by fat cells

the higher the insulin, the faster the glucose is vacuumed up by the GLUT 4 proteins in the muscles and fat cells

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GLUT 4  Insulin dependent

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GLUT 2

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GLUT 1

GLUT 1 not Insulin dependent

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Insulin Signaling GLUT 4 (4:10)

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GLUTS

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•  Females -‐-‐-‐ in the small intes?ne •  Males -‐-‐-‐ in the small intes?nes and testes

The more fructose we eat  the more GLUT 5 proteins we make.

Their GLUT protein works whether there is insulin or not and they have an enzyme ready to convert glucose into energy just to stay alive.

Pecking Order As insulin levels increase, fat and muscle cells get to dine because insulin triggers their GLUT proteins.

GLUT 1, GLUT 3, GLUT 4 proteins are not able to absorb fructose.

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Fructose goes straight to the Liver Fructose goes straight to the liver where it can be absorbed twice as quickly as glucose and it doesn’t have to wait for insulin.

The gut will process as much fructose as we put in our mouths

It has the enzyme fructokinase ready

with no known limit.

not insulin dependent.

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Fructokinase

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We can’t absorb fructose through our intes?ne unless we have GLUT 5 proteins there.

Brain cells and ordinary cells get to eat ﬁrst.

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the protein associated with the absorp?on of fructose

Pecking Order

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Fructokinase Fructose skips that regulatory step.

When fructokinase creates ATP, it bypasses the step in the glycolysis process which is controlled by PFK-‐1.

Usually when too much ATP is produced, PFK-‐1 switches oﬀ and controls the process.

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GLUT 5  Fructose

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Fructose is a Poison (8:01)

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Appetite Control

Insulin, lep?n and CCK tell us when we have had enough to eat.

Ghrelin temporarily inhibits the eﬀect of the other 3 and tells us that we need to eat.

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converted straight to faPy acids.

If we eat a high fructose diet, the fructose will be converted directly to faPy acids  body fat.

When we over-‐ consume fructose the loop-‐hole in our appe?te control mechanism opens up.

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Appetite Control All food we consume s?mulates the release of one or more of these hormones once we have had enough to eat.

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If we have lots of fructose in our blood, it rapidly overloads the ATP produc?on system of the liver

Fructose  Fatty Acids

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Fructokinase

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Fructose is invisible to the hypothalamus.

We can eat as much fructose as we like and never feel full for long.

Every gram of fructose we eat is directly converted to fat.

A small amount of fructose is OK.

It may help process glucose more eﬃciently.

However, consuming too much fructose overwhelms the body's capacity to process it.

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How much Fructose is OK?

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About 10% of the modern diet comes from fructose.

Our ancestors’ diets small amounts of fructose e.g. a handful of berries or a small amount of honey from a wild bee hive

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Ancestor’s Diet

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There is one substance which does not s?mulate the release of any of these hormones  FRUCTOSE

Fructose and Appetite Control

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The Problem is with too much! The liver starts making fats from fructose and sends them oﬀ into the bloodstream as triglycerides.

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Fructose and Appetite Control

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Excess fructose consump?on facilitates insulin resistance Metabolic Syndrome

Soft Drinks

The metabolism of fructose in the liver drives the produc?on of uric acid, which u?lizes Nitric Oxide, a key modulator of vascular func?on.

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Sog drinks are high in ‘High Fructose Corn Syrup’ (HFCS)

Excess fructose consump?on acid produc?on enzymes producing Nitric Oxide (NO)  Hypertension

High Fructose Corn Syrup (HFCS)

Fruits and vegetables have rela?vely small, "normal" amounts of fructose and most bodies can handle this.

The problem comes with added sugars.

HFCS is made up of 55% fructose and 45% glucose most ogen the culprit.

HFCS HFCS is a calorie-‐providing sweetener used in processed foods.

It is made by an enzyma?c process from glucose syrup derived from corn.

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 appe?te-‐regula?ng hormones (e.g. lep?n) are not triggered feel unsa?sﬁed

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Fructose circumvents the normal appe?te signaling system

Soft Drinks

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HFCS ( High Fructose Corn Syrup) is equally as sweet as table sugar blends well with other foods helps foods to maintain a longer shelf life is cheaper than other sweeteners

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High Blood Triglycerides

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sog drinks

processed foods

high uric acid produc?on gout

arthri?s

higher systolic BP

Metabolic Syndrome

stroke

All sugars are not used by the body in the same way. There are issues with fructose, which is treated diﬀerently by your body due to its eﬀect on insulin.

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In Summary

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Fructose Intolerance If you drink 300 ml of apple juice, you consume 300 calories.

100% fat free

no protein

14 gm fructose + 6 gm glucose

= 6 teaspoons sugar

+4 gm sucrose = 24 gm sugar

The 16 gm fructose is completely ignored by your pancreas.

The fructose is converted to approx 7 gm of fat (circula?ng faPy acids).

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Fructose Intolerance

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high consump?on of fructose

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almost all packaged foods have added fructose

fruit juice concentrates and sog drinks have a lot of fructose

High Consumption of Fructose

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Fructose -‐-‐-‐ undetected Fructose sugars go undetected by appe?te control mechanisms. (equivalent to ea?ng 5 whole apples) Your liver treats the fructose as fat  lots of free faPy acids circulate through the blood.

If you drink the same amount of milk, where all of the calories are recognized and treated as food, you will feel full.

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Fructose in our Food

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15 gm of body fat and the body only counts half the calories (140).

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A standard large sog drink (600 ml) contains 68 gm sugar and ½ is fructose. The 34 gm fructose is eﬃciently converted to

High fructose foods such as those with added fructose or HFCS have high levels of other sugars as well and contribute to insulin resistance.

Fresh fruit is OK because it is in its natural form -‐-‐-‐which keeps the GL down.

Your Bowel and Fructose Fructose intolerance is one cause of IBS, ﬂatulence and diarrhea, and a source of ‘whole body’ inﬂamma?on.

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Your Brain and Fructose Recent studies have found that concentrated fructose causes slowing of the brain func?on by slowing synap?c ac?vity.

Fructose slows the chemical transfer across the synapse.

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Fructose  Insulin Resistance

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The other 140 calories are completely ignored, giving the body permission to consume 140 more calories than one would otherwise normally eat in that meal.

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Fructose Malabsorption (FM) Too much fructose causes gastrointes?nal symptoms  approx 25% of the popula?on do not have the enzymes to absorb fructose.

An equal amount of glucose to fructose in fruit aids diges?on in the small intes?ne.

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More Maths!

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diarrhea bloa?ng gas

Gases from the large intes?ne created by undigested fructose cause an increase in hydrogen and methane which can be detected by a breath test.

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FODMAPs CHO’s poorly absorbed in the small intes?ne move through the diges?ve tract to the large intes?ne draw water into the colon and are rapidly fermented the fermenta?on of FODMAPs produces gas and other by-‐products

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FODMAPs

Many people with diges?ve disorders, such as IBS, ﬁnd that FODMAPs triggers symptoms including: abdominal pain

cramping

bloa?ng

excess gas

cons?pa?on

diarrhea

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FODMAPs

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cons?pa?on

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nausea

Fructose Malabsorption (FM)

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Gut Health & Hidden Food Intolerances Promote Inﬂammatory Cytokines

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A high fructose/ glucose ratio promotes FM.

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Some foods can produce an?bodies which circulate throughout the body and cause reac?ons up to 72 hours ager ea?ng.

Some?mes the diet may seem OK but reac?vity to foods may simmer away ‘under the radar’ causing inﬂamma?on and a mul?tude of symptoms

How do we test these foods? a two week elimina?on diet

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Hidden Food Intolerance

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to detox the body

• lactose and casein in milk • yoghurt •  cheese •  cream

Shell ﬁsh

Citrus fruits

Tomatoes

Soybeans

Eggs

•  shrimps • prawns

Nuts / Peanuts

Gut Bacteria Trillions of bacteria inhabit our bodies.

In our diges?ve tract we have more bacteria than cells in our bodies. Some of these are beneﬁcial to us, some are neutral and others are pathogenic.

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Dairy

•  ﬂour •  rye •  oats •  buckwheat

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Gut Bacteria Normally these maintain a symbio?c rela?onship with the host but:

poor diet

lifestyle

some medica?ons

can drama?cally diminish the levels of 'friendly' bacteria we have in our diges?ve tract and the result can be pathogenic and likely to cause leaky gut.

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Gluten

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Common Reactive foods

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draw out the culprits

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Gut Dysbiosis / Leaky Gut Dysbiosis  an imbalance of the bacteria in the gut

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Gut Dysbiosis / Leaky Gut Undesirable microbes ogen release poisonous chemicals such as: amines

ammonia

hydrogen sulﬁde

indoles

phenols

secondary bile acids

These microbes can damage the microvilli in the intes?ne and can be absorbed into the bloodstream causing a whole range of problems.

Gut Dysbiosis If the 'unfriendly' bacteria overwhelm the intes?nes this can compromise the immune system, which normally relies on some of the substances the friendly bacteria produce to operate eﬀec?vely.

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Leaky Gut (1.23)

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Gut Dysbiosis The microﬂora in the gastrointes?nal tract is also involved in:

synthesis of vitamins (B and K),

aiding gastrointes?nal tract mo?lity and func?oning

diges?on

nutrient absorp?on

inhibi?ng pathogens

metabolism of plant compounds / drugs

producing short chain faPy acids

producing polyamines

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which can result in a variety of chronic and degenera?ve diseases.

In_lamed Bowel  In_lamed Body

The presence of undesirable bacteria s?mulates produc?on of inﬂammatory cells

 travel throughout the body

inﬂammatory disease

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404

Our Mucosal Barrier strength of the mucosal barrier is compromised by loss of integrity of the ?ght junc?ons between each epithelial cell

increased intes?nal permeability

allows large molecules, an?gens and bacteria to cross the intes?nal membrane entering circula?on where the immune system is s?mulated Vojdani,A, 2009,‘Assessment of Intes?nal Barrier Permeability to Large An?genic molecules’ Biohealth Sta?s?cs

Our Mucosal Barrier

Inﬂammatory cytokines are then let loose to create inﬂamma?on throughout the body and may trigger autoimmune disease.

Vojdani,A, 2009,‘Assessment of Intes?nal Barrier Permeability to Large An?genic molecules’ Biohealth Sta?s?cs

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The Leaky Gut

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The abnormal bacteria in the intes?nes release exotoxins,

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Gut Dysbiosis

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Kelly, G, 1997, ‘Hydrochloric Acid: Physiological Func?ons and Clinical Implica?ons’, Alterna?ve Medicine Review

Primary Digestion

The presence of Helicobacter Pylori in the stomach is in ≈ 15% of the popula?on and it inhibits the produc?on of stomach acid.

Kelly, G, 1997, ‘Hydrochloric Acid: Physiological Func?ons and Clinical Implica?ons’, Alterna?ve Medicine Review

Small Intestinal Bacterial Overgrowth (SIBO) Bacteria from the large bowel may populate the small intes?ne or bacteria from foods ingested. Bacteria may not be eradicated in the stomach due to hypochlorhydria and pass on to the small intes?ne.

Inadequate: betaine

hydrochloride

in the stomach can result in malabsorp?on of essen?al nutrients such as: protein

magnesium

calcium

409

411

413

hypochlorhydria

iron

zinc

Kelly, G, 1997, ‘Hydrochloric Acid: Physiological Func?ons and Clinical Implica?ons’, Alterna?ve Medicine Review

Primary Digestion High carbohydrate diets inhibit gastrin which s?mulates the produc?on of betaine hydrochloride.

Beware clients on proton pump inhibitors PPI’s which shut down produc?on of stomach acid for GORD.

Kelly, G, 1997, ‘Hydrochloric Acid: Physiological Func?ons and Clinical Implica?ons’, Alterna?ve Medicine Review

Small Intestinal Bacterial Overgrowth (SIBO) The presence of bacteria in the small intes?ne interferes with diges?ve enzymes and malabsorp?on results. Integrity of the mucosal membrane in the small intes?ne is breached and larger food par?cles can enter the circula?on promo?ng an immune response.

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Primary diges?on in the stomach requires an adequate level of acidity to ini?ate break down of foods in prepara?on for ac?vity of the pancrea?c enzymes in the small intes?ne.

Primary Digestion

412

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Delivery of essen?al nutrients to the cells is cri?cal for eﬃcient repair post-‐injury and for maintenance of muscle integrity and strength.

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Primary Digestion

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lactose

lactulose

These ferment in the small intes?ne.

Consequently bacteria produces gas and the stomach bloats.

A compromised gut mucosal surface can become easily irritated from foods we don’t tolerate.

These food par?cles pass through our protec?ve barrier to underlying immune cells which produce an?bodies against that food.

Foods can provoke a variety of an?bodies:

IgE

IgG 1-‐4

They travel throughout the body causing global inﬂamma?on in: mucosal

membranes

muscles

joints

brain

416

Food Allergy/Intolerance Inﬂamma?on provokes a pain response.

Reac?ons can occur up to 72 hours ager ea?ng the food.

417

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Food Allergy/Intolerance

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419

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fructose

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A por?on of the popula?on do not have the enzymes to breakdown various sugars:

Food Allergy/Intolerance

418

Carbohydrate Maldigestion

When speciﬁc types of carbohydrates (disaccharides and polysaccharides) remain undigested in the intes?nes they provide fuel for bacteria and yeast.

as described by Dr Sidney Haas

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Small Intestinal Bacterial Overgrowth (SIBO)

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Excessive mucous produc?on results as the intes?nes react to the toxins, acids and undigested carbohydrates.

Endotoxins pass through the intes?nal endothelium and into the blood stream. Endotoxins s?mulate the produc?on of inﬂammatory mediators. Reducing the intake of high starch vegetables, complex carbohydrates and reﬁned sugars reduces the presence of undigested food in the intes;nes.

Pa?ents with IBS commonly have concurrent upper respiratory symptoms, reac?vity to environmental allergens and food allergies/intolerance. They will ogen present with heightened sensi?vity to light touch, mul?ple tender trigger points, and global pain.

Haas, SV et al. Am. J. Dis. Child 1924;28:421

IBS and Pain Some present with painful joints and some?mes with a diagnosis of inflammatory arthri?s. A strict an?-‐inflammatory elimina?on diet for two weeks can make a huge difference.

If the stomach is inﬂamed, eliminate food an?gens with an elimina?on diet for two weeks and test for Helicobacter Pylori.

Follow standard procedures for food challenges ager the ﬁrst two weeks.

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Suggestions to Heal the Gut and Aid Digestion

425

422

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Irritable Bowel Syndrome (IBS) and Pain

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The overgrowth of bad bacteria or candida can produce toxins and acids  injuring the lining of the small intes?ne.

Carbohydrate Maldigestion

424

Healing the Gut & Aid Digestion slippery elm

liquorice

marshmallow

ginger

aloe vera

querce?n

apple pec?n

L-‐Glutamine

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Carbohydrate Maldigestion

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Once the reac?vity in the stomach has sePled supplement with Betaine HCL to increase stomach acidity and improve primary diges?on.

Take into consideration:

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Suggestions to Heal the Gut and Aid Digestion?

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protein depriva?on lean muscle mass loss zinc and magnesium deﬁciency other signs of malabsorp?on

A dietary analysis to ascertain nutrient intake is useful. If the above protocol is unsa?sfactory you may need to recommend a test for bacterial overgrowth, candida or a parasite treat accordingly.

Dysbiosis Chronic Health Conditions Irritable Bowel Syndrome

Anklyosing Spondyli?s

Rheumatoid Arthri?s

Inﬂammatory Bowel Disease

Mul?ple Sclerosis

Chronic Fa?gue

Eczema

Fibromyalgia

Inﬂammatory Arthri?s

Food allergies

Many people are unaware that they are even suﬀering from Dysbiosis.

End of Day 1!

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431

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Recommend an appropriate probio?c for microbial balance in the large intes?ne.

428

430

Day 2

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Suggestions to Heal the Gut and Aid Digestion?

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427

432

Balance of macronutrients Signiﬁcance of micronutrients Cell func?on Protein synthesis Inﬂamma?on Metabolic Syndrome Diabetes / Insulin Resistance Fructose

Group Practical Session Carbohydrates

Protein

Fats

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Recap Day 1

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Gut Issues

Fibromyalgia Syndrome Signs and Symptoms Recognised pressure pain points A heightened response to painful s?muli Chronic fa?gue Sleep disturbance Joint s?ﬀness Bladder and bowel issues Diﬃculty swallowing Numbness and ?ngling Cogni?ve dysfunc?on Depression Anxiety Post trauma?c stress Brain func?onal and structural changes

435

“a central sensi?za?on syndrome"caused by neurobiological abnormali?es which act to produce physiological pain and cogni?ve impairments as well as neuro-‐psychological symptomatology.”

John Winﬁeld MD, ‘Fibromyalgia (Deﬁni?on and Pharmaceu?cal approach)’

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Fibromyalgia: What is it?

436

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Fact or Fic?on

434

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Fibromyalgia

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437

438

John Winﬁeld MD, ‘Fibromyalgia (Deﬁni?on and Pharmaceu?cal approach)’ hPp:// emedicine.medscape.com/ar?cle/329838-‐clinical#a0256

Reported Concomitant Fibromyalgia Symptoms 20% of people with ﬁbromyalgia have concomitant restless legs syndromebrain micronutrients?

439

John Winﬁeld MD, ‘Fibromyalgia (Deﬁni?on and Pharmaceu?cal approach)’ hPp:// emedicine.medscape.com/ar?cle/329838-‐clinical#a0256

Reported Concomitant Fibromyalgia Symptoms 40% of pa?ents with ﬁbromyalgia describe having alterna?ng bouts of diarrhoea and cons?pa?on and also experience bloa?ng, cramping, and an increased urge to defecateirritable bowel?

Reported Concomitant Fibromyalgia Symptoms Many pa?ents with ﬁbromyalgia report that fa?gue is second only to pain as a source of distress. The fa?gue is worse in the morning and early evening. By 10 or 11 am the fa?gue subsides adrenal fa?gue?

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Most pa?ents awaken frequently throughout the night, and some have diﬃculty falling asleep.

They ﬁnally fall asleep in the early morning hours, describing this as their best sleep”

440

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“Pa?ents generally do not volunteer a history of a sleeping disorder, but a carefully taken history reveals ‘unrefreshing sleep’ in about 65% of pa?ents and morning fa?gue in about 80%.”

Fibromyalgia and Sleep

442

Reported Concomitant Fibromyalgia Symptoms mood and anxiety disorders

Cogni?ve symptoms include: confusion

forge‰ulness

inability to concentrate

Weight ﬂuctua?ons Sugar metabolism/cor?sol? Allergic symptoms Bowel dysbiosus?

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Pa?ents awaken as ?red as they were before sleeping.

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Fibromyalgia and Sleep

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≈25% of pa?ents with RA and approx 50% of pa?ents with SLE also have ﬁbromyalgia 443

444 John Winﬁeld MD, ‘Fibromyalgia (Deﬁni?on and Pharmaceu?cal approach)’

Maldiges?on / malabsorp?on of essen?al nutrients for muscle relaxa?on and ac?va?on

Gut dysbiosussmall intes?nal bacterial overgrowth (SIBO)

Nutrient deﬁciency aﬀec?ng neurotransmiPer status

Sleep depriva?on / sleep apnoea

Stress -‐-‐-‐ the HPA axis and adrenal fa?gue

Altered EFA status eﬀects cell membrane integrity

Hormonal changes -‐-‐-‐ hypothyroidism or haemachromatosis

paPerns rela?ng to underlying biomechanical dysfunc?on, acupuncture channels or internal organ disturbance?

Trigger points

Chronic Fatigue Syndrome

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446

Chronic Fatigue Syndrome With Chronic Fa?gue Syndrome, energy demand quickly exceeds the supply of ATP

Cells start to convert ADP to AMP (1 phosphate) for energy.

AMP cannot be converted back to ADP or ATP so it is lost in the urine

ATP has to be made from raw ingredients which takes up to a few days

delayed fa?gue experienced with CFS

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447

Chronic Fatigue Syndrome

449

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Mitochondrial dysfunc?on

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Chronic inﬂamma?on and /or infec?on

Fibromyalgiapossible underlying triggers

448

Chronic Fatigue Syndrome The body can make a small amount of ATP direct from glucose (via pyruvate).

This is anaerobic and the bi-‐product is lac?c acid which builds up in the muscles causing pain with fa?gue.

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Fibromyalgia-‐ possible underlying triggers

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(oxida?ve stress-‐induced damage) decreased high levels of reduced levels levels of mitochondrial of CoQ10 and CoQ10 and reac?ve mitochondrial ATP compared oxygen DNA contents with controls species (ROS)

Castro-‐Marrero, Cordero et al, 2013. ‘Could Mitochondrial Dysfunc?on Be a Diﬀeren?a?ng Marker Between Chronic Fa?gue Syndrome and Fibromyalgia?’ An?oxidants & Redox Signaling

(Tumour Necrosis Factors refer to a group of cytokines which can cause cell death)

Castro-‐Marrero, Cordero et al, 2013. ‘Could Mitochondrial Dysfunc?on Be a Diﬀeren?a?ng Marker Between Chronic Fa?gue Syndrome and Fibromyalgia?’ An?oxidants & Redox Signaling

Statins, CoQ10 & Mitochondrial

Dysfunction Moderate doses of both Simvasta?n and Pravasta?n were associated with ?redness and exer?on fa?gue  CoQ10 deﬁciency?

It is es?mated that fa?gue could aﬀect between 20% and 40% of pa?ents taking sta?ns.

Hamilton-‐Craig, I, ‘Sta?n-‐associated myopathy’, Australian Prescriber, 2003;Vol 26,PP 74-‐5 Cordero et al, 2013 ‘Can Coenzyme Q10 Improve Clinical and Molecular Parameters in Fibromyalgia?’ An?oxidants & Redox Signaling April 6 online ed

453

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Signiﬁcant nega?ve correla?on between CoQ10 and TNF-‐α levels.

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451

CFS and Fibromyalgia Patients

455

high levels of serum tumour necrosis factor (TNF)-‐α

In_lammation and Fibromyalgia

A signiﬁcant nega?ve correla?on was found between CoQ10 and TNF-‐α levels.

A signiﬁcant posi?ve correla?on was found between reac?ve oxygen species and TNF-‐α levels.

Codero et al, 2012. ‘Is Inﬂamma?on a Mitochondrial Dysfunc?on-‐Dependent Event in Fibromyalgia?’ An?oxidants & Redox Signalin

Statins, CoQ10 & Mitochondrial

Dysfunction Evidence suggests muscular pain can also relate to deple?on of CoQ10 from muscles due to sta?n use.

(While sta;ns inhibit the produc;on of cholesterol in the liver, they also inhibit the produc;on of CoQ10.) Hamilton-‐Craig, I, ‘Sta?n-‐associated myopathy’, Australian Prescriber, 2003;Vol 26,PP 74-‐5 Cordero et al, 2013 ‘Can Coenzyme Q10 Improve Clinical and Molecular Parameters in Fibromyalgia?’ An?oxidants & Redox Signaling April 6 online ed

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If there is limited ATP available, lac?c acid is not cleared and the pain persists.

Signiﬁcantly higher levels of lipid peroxida?on

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Two molecules of ATP are produced from glucose when converted to lac?c acid by glycolysis, but it takes six molecules of ATP to convert it back via the Cori cycle in the liver.

CFS and Fibromyalgia Patients

454

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Chronic Fatigue Syndrome

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Mitochondrial Function and Cofactor Nutrients

The mitochondria produces ATP in two ways: Krebs citric acid cycle tricarboxylic acid cycle

90% of energy from food, (carbohydrate, fats and protein) is produced via the Krebs Cycle.

exhaus?on

cancer

myopathy

depression resistant to an?-‐ depressants

high blood pressure

gum disease and tooth loss

hair loss

liver disease

sudden complete memory loss or amnesia

cataracts

angina, cancer

folic acid deﬁciency

damaged cell membranes 458

Mitochondrial Function and Cofactor Nutrients Through a series of enzyma?c reac?ons it comes out as 3CO2, 4NADH, FADH2 and one ATP.

Glucose can be sourced directly from carbohydrates or from protein and fats by gluconeogenesis in the liver.

459

460

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At ?mes of O2 debt, pyruvate is converted to lac?c acid.

conges?ve heart failure

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The Krebs cycle is aerobic requiring O2.

heart aPack

457

Pyruvate is produced from glucose by the process called glycolysis enters the citric acid cycle as acetyl CoA

Krebs Cycle

fatal cardiomyopathy

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Reduc?on in pain, fa?gue, and morning ?redness was achieved with supplementa?on with CoQ10 in ﬁbromyalgia pa?ents.

CoQ10 De_iciency

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Dysfunction

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Statins, CoQ10 & Mitochondrial

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462

Cofactors needed in the Krebs cycle are Vitamins B1,B2,B3 & B5 plus magnesium.

No sta?s?cally signiﬁcant correla?ons were found between mean levels of serum Vitamins A, C, E, and Mg in another study.

(not looking at ;ssue levels here)

Kim, YS, 2011. ‘Women with fibromyalgia have lower levels of calcium, magnesium, iron and manganese in hair mineral analysis.’ J Korean Med Sci. 2011 Oct;26(10):1253-‐7 Bagis , S, 2013. ‘Is magnesium citrate treatment effec?ve on pain, clinical parameters and func?onal status in pa?ents with fibromyalgia?’ Rheumatol Int. 2013 Jan;33(1):167-‐72. Sakarya ,ST, 2011. ‘The rela?onship between serum an?oxidant vitamins, magnesium levels, and clinical parameters in pa?ents with primary fibromyalgia syndrome.’ Clin Rheumatol. 2011 Aug;30(8):1039-‐43.

Magnesium and Fibromyalgia

Early studies found that the most eﬀec?ve way to reduce muscle pain in ﬁbromyalgia was to address the cellular fa?gue.

Magnesium deﬁciency may reduce physical performance and reduce exercise capacity.

463

Magnesium is critical for Energy Production Magnesium is involved in many cellular reac?ons.

Most ATP in cells is bound to Mg2+.

Therefore energy produc?on and transport in muscle, and the ability to maintain a contrac?on requires Magnesium.

465

464

466 McCully,K, 2006, ‘Increase of free MG2+ in the skeletal muscle of chronic fa?gue syndrome pa?ents.’ Dynamic medicine 5:1

Magnesium and Fibromyalgia

Diets high in reﬁned sugars and alcohol are not only lacking adequate Magnesium content, but deplete ?ssue Magnesium stores.

• Bohl, C, 2002. ‘Magnesium and Exercise’ Crit Rev Food Sci Nut 42(6):533-‐563 Bohl, C, 2002. ‘Magnesium and Exercise’ Crit Rev Food Sci Nut 42(6): Dreos?, I, 1995, ‘Magnesium status and health’ Nutri?on reviews, Washington:

Magnesium transfers phosphates from ATP to ADP and back again.

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The serum and erythrocyte Magnesium levels were signiﬁcantly lower in pa?ents with ﬁbromyalgia than in the controls.

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Minerals and Fibromyalgia

There is a deﬁcit of Magnesium ager moderate exercise thought to be due to eﬄux of Magnesium from cells ager muscle breakdown.

467

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The concentra?ons of Calcium, Magnesium, Iron, and Manganese in the hair of female pa?ents with ﬁbromyalgia are lower than of controls.

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Minerals and Fibromyalgia

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•  Expression of mitochondrial DNA •  Mitochondrial complexes •  FaPy acid oxida?on •  Oxygen consump?on

Neuron RNA oxida?on •  Oxida?ve stress

Serum glutathione and catalase levels have been found to be signiﬁcantly lower in ﬁbromyalgia pa?ents than controls.

No signiﬁcant diﬀerence was seen in serum NO levels between the two groups.

A signiﬁcant correla?on was evident between serum NO level and pain.

469

470 Sendur, O et al. 2009, ‘Serum an?oxidants and nitric oxide levels in ﬁbromyalgia: a controlled study.’ Rheumatol Int. 2009 Apr;29(6):629-‐33

A correla?on between glutathione level and morning s?ﬀness was found.

They concluded that a deﬁciency of these two an?oxidants may impact on the pathogenesis of ﬁbromyalgia.

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Shen, W et al, 2008, ‘R-‐alpha-‐Lipoic acid and acetyl-‐L-‐carni?ne complementarily promote mitochondrial biogenesis in murine 3T3-‐L1 adipocytes.’ Diabetologia Vol 51, 165-‐174.

Antioxidant Levels and Fibromyalgia

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Mitochondrial mass

Antioxidant Levels and Fibromyalgia

Check for Metals

Cu / Zn imbalance

Cadmium

Mercury

Arsenic

Lead

Aluminum

Trabizian, I, ‘Visual Textbook of Nutri?onal Medicine’ NRS Publica?ons Educa?onal Serie

471

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Lipoic Acid & Acetyl-‐L-‐Carntine

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Magnesium

Zinc

Iron

Selenium

Calcium

Boron

Folate

Molybdeum

Vitamins B’s, C, D &E

Mercury

Mercury ﬁllings can leak Mercury into the ?ssues causing oxida?ve stress and damage to mitochondrial DNA, lipids and proteins, and possibly mitochondrial death.

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These Metals may block the action of:

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Sendur, O et al. 2009, ‘Serum an?oxidants and nitric oxide levels in ﬁbromyalgia: a controlled study.’ Rheumatol Int. 2009 Apr;29(6):629-‐33

Manganese

473

474

Weatherby, D & Ferguson, S, 2009, ‘Blood Chemistry and CBC Analysis’

Mercury also inhibits molecular transport across the mitochondrial membrane and deac?vates enzymes of the electron transport chain.

475

476

Weatherby, D & Ferguson, S, 2009, ‘Blood Chemistry and CBC Analysis’

Muscle fa?gability is associated with enhanced produc?on of reac?ve oxygen species, increased mitochondrial apoptosis and reduced mitochondrial biogenesis.

Weatherby, D & Ferguson, S, 2009, ‘Blood Chemistry and CBC Analysis’

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Mercury

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Mercury aﬀects the absorp?on of B vitamins necessary for energy produc?on.

Mercury

Pharmaceutical Treatments “The physician should inform the pa?ent that no cure exists for ﬁbromyalgia” John Winﬁeld MD

Doctors prescribe medica?ons such as: jurnista (opioids)

an?-‐depressant medica?ons (SSRI’s), amitriptyline, duloxe?ne

pregabalin (Lyrica)

477

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Mercury

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478

The number of pa?ents needed to treat (NNT) to get 50% reduc?on in pain is between 3 and 11.

479

Dextromethorphan

an N -‐methyl-‐D-‐aspartate (NMDA) receptor antagonist, available as an over-‐the-‐counter an?tussive, is used as an adjunc?ve therapy in pa?ents with ﬁbromyalgia

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Needed to Treat (NNT)

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Weatherby, D & Ferguson, S, 2009, ‘Blood Chemistry and CBC Analysis’

480

Stronger Opioid medica?on is ogen prescribed by a pa?ent’s GP but it ogen does not provide eﬀec?ve pain relief.

Raloxifene (Evista)

oral selec?ve oestrogen receptor modulator (SERM) with oestrogenic ac?ons on bone and an?-‐oestrogenic ac?ons on the uterus and breast

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481

482

Raloxifene (Evista)

used in the preven?on of osteoporosis in postmenopausal women

found to improve pain and fa?gue

reduces the tender point count in postmenopausal women with ﬁbromyalgia symptoms

What is the connec?on between hormonal imbalance and ﬁbromyalgia symptoms?

Could it be the link between low oestrogen and serotonin?

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483

Pharmaceutical Treatments

485

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High doses cause hyperalgesia.

They may prescribe NSAID’s for the pain of concurrent inﬂammatory condi?ons such as arthri?s.

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a weak opioid agonist with addi?onal eﬀects on serotonin and norepinephrine receptors, improves pain associated with ﬁbromyalgia

Pharmaceutical Treatments

484

Pharmaceutical Treatments

These medica?ons have been shown to reduce the symptoms of fibromyalgia but there are side effects and are they pu•ng out the fire within?

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Tramadol

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486

Problems arise when the pa?ent is not producing enough serotonin.

487

Pregabalin is a structural deriva?ve of GABA but it’s ac?on is unknown.

An?convulsants are used to treat chronic pain and neuropathic pain and serve as adjunc?ve medica?ons for sleep disturbance and depression.

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Pharmaceutical Drugs Biochemistry

Amitriptyline and Duloxe?ne inhibit the re-‐uptake of serotonin and/or norepinephrine at the presynap?c neuronal membrane.

488

Neurotransmitters and Pain Perception What happens at the nerve synapse? Which neurotransmiPers are involved with pain signaling? Essen?al nutrient cofactors make neurotransmiPers for pain relief... How does sleep eﬀect pain and repair? The 24 hour body clock...

Synaptic Release of the Neurotransmitters Vesicles containing the neurotransmiPer fuse with the plasma membrane and release contents into the synapse.

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489

490

Video of a Synapse (2.43)

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SSRI’s slow down the uptake of serotonin in the synapse to prolong it’s inhibitory eﬀect on pain transmission.

Biochemistry of Pharmaceutical Drugs

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Biochemistry of Pharmaceutical Drugs

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NeurotransmiPer molecules diﬀuse to and bind to receptors on the postsynap?c neuron (exi?ng nerve).

491

492

The membrane of the terminal buPon is depolarised by the arriving ac?on poten?al opens calcium channels on the presynap?c membrane.

Note that a calcium deﬁciency can interfere with genera;on of the synap;c poten;al

Calcium ions inﬂux through the membrane.

The neurotransmiPer is then removed by reuptake or is destroyed by enzymes. SSRI’s inhibit the reuptake of serotonin.

Adenosine the sleep molecule of the brain ATP is released from healthy cells at ?mes of stress -‐-‐-‐ mechanical deforma?on, swelling or hypoxia -‐-‐-‐ not just from damaged or dying cells.

494

Generation of the Post-‐Synaptic Potential Excitatory neurotransmiPers create an ac?on poten?al by depolarising the post-‐synap?c membrane

(inﬂux of Na+ ions)

Inhibitory neurotransmiPers inhibit the post-‐synap?c membrane with an inﬂux of chloride ions or eﬄux of potassium ions

495

ATP is rapidly degraded by enzymes to adenosine. 497

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The ac?on of the sum of neurotransmiPers in the synapse produces either depolarisa?on (excitatory) or hyperpolarisa?on (inhibi?on) of the post-‐ synap?c membrane.

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Interac?on is like a ‘key ﬁ•ng into a lock’

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493

Generation of the Post-‐ Synaptic Potential

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What Happens at the Nerve Synapse?

496

Adenosine Accumula?on of adenosine with loss of energy and ATP s?mulates the need to rest and sleep to recover energy stores. Adenosine is considered a sleep promo?ng substance which inhibits cholinergic wake promo?ng neurons. Note: coﬀee consumed in the evening can counter the eﬀect of adenosine.

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498

There are separate purinoceptors for adenosine and mul?ple variables of ATP or ADP receptors.

ATP is the transmiPer of nocicep?on in the gut and bladder ac?vated by distension of the lumen wall.

Adenosine and Pain ATP s?mulates glutamate release and both are primary co-‐transmiPers in primary aﬀerent central nerve terminals, and have been implicated in neuropathic pain. ATP produced ager ?ssue stress to the musculoskeletal system excites myofascial nociceptors. ATP increases intracellular Ca2+ in neurones and glia of the dorsal spinal cord thereby crea?ng excita?on of dorsal horn neurones.

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Adenosine and Pain ATP acts post synap?cally on various P2X receptors promo?ng interleukin-‐1B release, brain derived neurotrophic factor (BDNF), and transcrip?on factor cyclic-‐AMP. ATP is released with norepinephrine and neuropep?de Y from sympathe?c nerves and poten?ates pain behaviour.

Adenosine acts on sensory terminals.

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Adenosine and Pain

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ATP is a co-‐transmiPer in both the peripheral and central nervous systems.

Ini?a?on of nocicep?on in the periphery is relayed in the spinal cord by purinergic receptors on small nociceptor sensory nerves in the dorsal root ganglia.

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Receptors for purines and pyrimidines are throughout the body on neuronal and non-‐neuronal ?ssue.

Adenosine and Pain

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A1 Receptors A1 receptors suppress pain signaling while A2 receptors facilitate pain signaling.

A1 receptors are more prevalent than A2 receptors.

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Adenosine and Pain

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A1 receptors mainly exert an inhibitory eﬀect on glutamate release and therefore reduces neuronal excitability G Burnstock & J Sawynok ‘Adenosine Triphosphate and Adenosine Receptors and Pain’ Autonomic Neuroscience Centre, University College Medical School London, and Dept Pharmacology, Dalhousie Univ Halifax, Canada

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reduce cyclic AMP

reduce pep?de release in sensory nerves

reduce protein kinase A ac?vity

increase K+ conductance and hyperpolaris ac?on of dorsal horn neurons.

Peripheral administra?on of A1 agonists has produced an?nocicep?on of mechanical and thermal hyperalgesia.

Adenosine dampens inﬂamma?on.

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G Burnstock & J Sawynok ‘Adenosine Triphosphate and Adenosine Receptors and Pain’ Autonomic Neuroscience Centre, University College Medical School London, and Dept Pharmacology, Dalhousie Univ Halifax, Canada

Adenosine Application Sublingual for rapid absorp?on to the CNS will induce ?redness in prepara?on for sleep.

IV administraEon is used for neuropathic pain.

Intramuscular injecEon for varicose veins and local symptoms

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reduce Ca2+ ions entry at the synapse

Adenosine and Pain

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A1 Receptors

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an inhibitory neurotransmiPer most ac?ve in wake ?mes facilitates relaxa?on during the day and helps prepare us for sleep by reducing sensory input and inhibits muscle ac?vity inhibits messages coming to the brain from the body including sensi?vity to touch, pain and muscle tension concentrated in the pineal gland for the produc?on of melatonin mostly used in the gut wall for relaxa?on of muscles. Cordero et al. 2010 ‘Low levels of serotonin in serum correlates with severity of ﬁbromyalgia.’ Med Clin. Nov 13;135(14):644-‐6.

Hormonal In_luences on Serotonin Oestrogen receptors E2α and E2β play a role in regula?ng serotonin. E2 increases produc?on of tryptophan hydroxylase, the rate-‐limi?ng step in the synthesis of serotonin from tryptophan Oestrogen suppresses ac?vity of monoamine oxidase type A and increases type B enzymes in neuron synapses increased levels of adrenaline, noradrenaline and serotonin.

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Serotonin

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Courtesy G Burnstock & J Sawynok University College Medical School London

510 Ann Vlass, ‘Oestrogen’s inﬂuence on anxiety and depression’ BioConcepts Educa?on Centre

Increased awake ?me at night

Panic aPacks

Aggressiveness

Sugar and alcohol cravings

Depression Ea?ng disorders

Emo?onal instability

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Osiecki, H, & Samvat, R, 2009, ‘Sleep, Health & Consciousness, A Physician’s Guide’, Bio Concepts Publishing, Eagle farm, QLD, Australia

Serotonin Production Serotonin is produced from L-‐tryptophan via 5-‐ hydroxytryptophan, and the precursors are magnesium, iron, calcium, folic acid, Vitamin B6 and zinc. Low levels of Vitamin B3 will s?mulate transforma?on of tryptophan to niacin (Vitamin B3) When aPemp?ng to increase the conversion of tryptophan to serotonin, Vitamin B3 should also be supplemented. Juhl, J, 1998, ‘Fibromyalgia and the Serotonin Pathway’ Alterna?ve Medical review, Vol 3, No 5, p367-‐375.

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Serotonin deﬁciency is also implicated in emo?onal disorders such as depression, suicide, and aggression

Diﬃculty ge•ng to sleep

Anxiety

Ann Vlass, ‘Oestrogen’s inﬂuence on anxiety and depression’ BioConcepts Educa?on Centre

A low serotonin level has been implicated as causal factor ﬁbromyalgia. Serotonin levels were decreased by 45% compared to healthy individuals.

Increased reac?vity in the muscles

Irritability

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Serotonin De_iciency

Increased pain sensi?vity

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High levels of the stress hormone cor?sol block oestrogen and progesterone receptor func?on  reduces serotonin levels with increased serotonin re uptake and degrada?on of tryptophan down the kynurenine pathway

Low self-‐ esteem

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E2 inhibits gene expression of the serotonin re uptake transporter  more serotonin available in the synapse.

Serotonin De_iciency

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GABA Gama-‐aminobutyric acid (GABA) is a powerful inhibitory neurotransmiPer in the brain and throughout the central nervous system.

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Hormonal In_luences on Serotonin

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GABA

Correla?ons between clinical pain severity and concentra?ons of the excitatory amino acid neurotransmiPer glutamate have been demonstrated in ﬁbromyalgia suﬀerers.

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GABA Magnesium also competes for NMDA receptors to prevent calcium entry into the neuron and reduces glutamate toxicity

The opioids enkephalin and endorphins provide a ‘feel good’ pleasure eﬀect and ease pain. Because opiates are used in sleep regula?on as well, low levels are another reason why pain suﬀerers have disrupted sleep.

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Opioids

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Pain can be a learned response. A long dura?on of chronic pain s?mulates the glutamate receptor, the NMDA receptor in the post synap?c neurones in the brain.

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GABA blocks the release of other neurotransmiPers and promotes deep repara?ve sleep, non-‐REM sleep. It is also important for muscle relaxa?on.

GABA

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Opioids Serotonin s?mulates the release of opioids. Low serotonin, considered to be one causa?ve factor in depression, is therefore associated with low endorphins and heightened pain.

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GABA

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Dx: Fibromyalgia by Rheumatologist 2 years previous First impression is of normal appearance, not obviously under or over-‐weight

Body composi?on:34.4% body fat, 37.6kg lean mass (~8-‐10 kg loss), Bone mass 2.0 (average for women 55-‐75 kg is 2.40), hydra?on 47.5%

Tongue scalloped edges and red ?p deﬁcient B Vitamins, 3, 6 or 12 Bowel mo?ons: 1-‐2 per day mostly formed and dark. Zinc taste test: slightly furry ager 10 seconds indicates zinc deﬁciency Zinc and Vitamin B6 are required for protein synthesis and manufacture of neurotransmiPers

Calcium/Magnesium balance This lady drank 2 glasses of wine daily.

Alcohol is a drug known to deplete magnesium stores. It upsets the balance between magnesium and calcium. The low levels of cellular Mg2+ result in disturbance of cytoplasmic and mitochondrial pathways, e.g. low magnesium to mediate ADP to ATP in the Krebs cycle.

This could be one issue contribu?ng to her fa?gue.

Low protein and zinc will deplete Magnesium as well -‐-‐-‐ Type 2 nutrient deﬁciency.

Fear of pain aggrava?on with ac?vity / pain memory IntermiPent depression  not medicated Sleep: no diﬃculty falling asleep but could wake on occasion with hot ﬂushes then cold.

No complaint of diges?ve symptoms but unable to eat a large por?on of meat.

Her Diet She ate meat a few ?mes per week, average protein intake was 51gm per day measured over 4 days She avoided wheat/gluten Drinks 2 glasses wine per day Computerised diet analysis: • Total energy 5061 kj • Poly unsaturated fats -‐-‐-‐ 4.6gm (low) • 48% carbs, 21% protein, 15% fats, 16% alcohol • Intake low in calcium, magnesium, zinc, B1,2,5,6 &12. Also very low sodium intake • Very high Vitamin A intake.

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N.B. Balance between Vitamins D and A for bone health

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Prolonged capillary flush on the fingers  protein deficiency

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Thin ﬂaky nails, no white spots on nails but ver?cal ridges  protein and EFA deﬁciency

Muscle fa?gue ager minimal exercise and sog ?ssue massage, with persistent aches for a week agerward

Poor dream recall deﬁcient Vitamin B6

Closer examina?on: signiﬁcant muscle was?ng especially back and shoulders

Case Study O/E

Post-‐menopausal ≈ 5 yrs

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PPx: Burning / persistent ache both sides neck and shoulders

Case Study C/0

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Female 55 years, Height 174cm, weight 60 kg

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What to Check Dietary insufficiency Hydrochlorhydria Malabsorp?on Pancrea?c insufficiency (diges?ve enzymes) EFA imbalance Liver detoxifica?on pathways Zinc/Cu imbalance. Metal toxicity

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Case Study -‐-‐-‐ Mrs. S

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Vitamin D status Mitochondrial nutrients

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Severe protein deﬁciency-‐synthesis, diet or diges?on?

Probable mul?ple micronutrient deﬁciency including magnesium, calcium, zinc and mitochondrial nutrients

Type 2 nutrient deﬁciency:

Amino acids, Mg, Zn, K, Phos, Sulphur, Sodium

Summary of Pathology and Examination Diet deficient in many essen?al nutrients Pain aggravated by light massage Significant muscle was?ng Zinc taste test showed she was deficient Low protein synthesis -‐-‐-‐ she is zinc deficient and has no dream recall indica?ng low Vit B6. Zinc and Vit B6 are also cofactors for produc;on of stomach acid.

Her protein intake could be higher but consider diges?on/ absorp?on.

Low blood urea and crea?nine and low-‐normal albumin are indicators of low protein status. MCV macrocy?c over a number of years-‐ Deﬁcient B12, Folate or protein  ask doctor to check Homocysteine Low range serum B12 and Folate

Low serum calcium and low intake

Low iron stores (ferri?n), Low Vitamin D

Likely low B vitamins and EFA’s (required for cellular energy)

To improve lean muscle mass is a priority therefore she needs 80-‐90gm protein per day with protein at every meal

Consequences of Low Protein Status

A loss of lean body mass results from increased uptake of amino acids from muscle in an aPempt to make up for insuﬃcient amino acids derived from protein in her diet, hence a nega?ve nitrogen balance exists.

Fa?gue results from poor contrac?le strength in the muscles and ﬂows on to poor exercise tolerance

Consequences of Low Protein Status

Low urea and crea?nine indicate that she has limited protein to be used for energy and her body is aPemp?ng to hold onto it’s amino acid/ nitrogen stores.

A low level of the albumin would therefore reduce her ability to u?lize these essen?al nutrients for cellular func?on, energy produc?on and mul?ple enzymes.

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Summary of Pathology and Examination

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Priorities of Treatment First priority is to manage her diet, increase protein and fresh vegetables at every meal. Her fruit intake was good. Assist primary diges?on and diges?ve enzymes. Even though she did not complain of diges?ve symptoms, she did report some difficulty ea?ng protein foods and lacks the cofactors zinc and B6 to produce sufficient stomach acid to synthesize proteins. Avoid alcohol and coffee.

Type 2 nutrient deﬁciency therefore supplement Magnesium with Zinc together. Her alcohol intake would deplete these.

Consider mitochondrial nutrients.

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•  B12/Folate deﬁciency -‐-‐-‐ MCV is macrocy?c (100) •  Mul?ple neurotransmiPer deﬁciency

Albumin is a transporter protein in the blood that transports a variety of nutrients such as calcium, zinc and Vitamin B6.

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What do we Suspect?

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Weekly B12 injec?ons may be of beneﬁt  doctor

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Ω3 oil to provide energy at the cellular level, improve cell membrane ﬂuidity and displace arachidonic acid from the membranes and reduce inﬂamma?on Reassess pain levels and sleep for need to add other neurotransmiPer cofactors, eg GABA Hormones  doctor to assess adrenal hormones Cor?sol / DHEA balance, and Steroid hormones. Low DHEA and steroid hormones can increase protein ;ssue catabolism.

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By improving her dietary protein intake and diges?ve support at every meal; supplemen?ng with zinc and ac?vated B vitamins for protein synthesis and cellular energy, and magnesium for muscle energy and relaxa?on, she had signiﬁcant changes to her symptoms.

Check out the pain paPerns for clues to inner health disturbance. Work through the basics of diet, diges?on, absorp?on, gut health and food intolerances. Support bowel ﬂora and liver detoxiﬁca?on. Consider environmental factors. Counsel on lifestyle factors: work, stress, sleep & ea?ng habits.

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Treatment Outcome for Mrs. S

Take a full history. Look for clues of nutrient deﬁciency in skin, hair, nails, tongue, muscle bulk etc.

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For pain  querce?n, curcumin

In Summary No recipe

Supplement to balance micronutrients and neurotransmiPer cofactors as required.

Treatment Outcome for Mrs. S Her pain sePled by 80%

She tolerated some gentle isometric strengthening exercises and began walking 5-‐10 minutes per day.

Over the next 6 weeks she steadily improved her exercise tolerance and was sleeping through the night.

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Treatment Support

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She was so happy that no further inves?ga?on or treatment was needed.

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Cholesterol Essen?al for your health

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Morning Tea

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forms membranes surrounding cells

maintains cellular ‘waterprooﬁng’ so diﬀerent chemical reac?ons can take place inside and outside the cell

The Importance of Cholesterol

The ability to grow new synapses in the brain depends on the availability of cholesterol latches cell membranes together so that signals can easily jump across the synapse.

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Lipoproteins Cholesterol is insoluble in water and also in blood transported in our blood inside spheric par?cles composed of fats and proteins. (lipoproteins)

Lipoproteins are easily dissolved in water because their outside is composed mainly of water-‐soluble proteins.

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It’s crucial to understand that you don’t have a cholesterol level in your blood

keeps cell membranes permeable

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Understanding Cholesterol (2:16)

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Cholesterol is fat soluble Cholesterol is technically not a fat. It is a sterol  a combina?on of a steroid and alcohol

The Function of Cholesterol

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Cholesterol

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Like submarines, lipoproteins carry cholesterol from one place in the body to another.

LDL & HDL Lipoproteins, have various names according to their density.

HDL (High Density Lipoprotein)

LDL (Low Density Lipoprotein)

HDL The main task of HDL is to carry cholesterol from the peripheral ?ssues, including the artery walls, to the liver.

It is excreted with the bile, or used for other purposes, for instance as a star?ng point for the manufacture of important hormones.

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LDL LDL’s mainly transport cholesterol in the opposite direc?on.

They carry it from the liver, where most cholesterol is produced, to the peripheral ?ssues, including the vascular walls.

When cells need cholesterol, they call for the LDL’s, which then deliver cholesterol into the interior of the cells.

LDLBad? LDL is not bad unless it is oxidized  inﬂammatory! Insulin is the number one indicator for inducing inﬂamma?on of blood vessels.

The oxida?on of LDL occurs when the LDL cholesterol par?cles in your body react with free radicals.

The oxidized LDL’s then become more reac?ve with the surrounding ?ssues  ?ssue damage.

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The inside of the lipoproteins is composed of lipids, and there is room for water-‐ insoluble molecules such as cholesterol.

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Measuring Lipoprotein Levels the total LDL and HDL cholesterol is measured

indicates the concentraEon of cholesterol inside of the lipoproteins

what should be measured is the number of LDL par?cles in the blood

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Lipoproteins

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the more collisions into the arterial wall

the more damage and inﬂamma?on

the more par?cles

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Cholesterol for the Brain crucial component in the myelin coa?ng around the neuron, allowing quick transmission of informa?on

acts as a facilitator for the brain to communicate and func?on properly

serves as a powerful an?oxidant, protec?ng the brain against damaging eﬀects of free radicals

The fundamental role of LDL in the brain is to capture cholesterol and transport it to the neuron to perform cri?cally important func?ons.

When cholesterol levels are low, the brain simply doesn’t work well and individuals are at a signiﬁcantly higher risk of developing neurological problems.

Sugar can also render it dysfunc?onal by accelera?ng oxida?on. Oxidized LDL  atherosclerosis

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LDL and the Brain

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The blood carrying lipoproteins is in constant contact with the endothelial lining. So why does the LDL par?cle leave the blood, penetrate the endothelium and enter the artery wall? The answer is that it’s a gradient-‐driven process.

Gradient Effect

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Coronary arteries are hollow tubes, and the endothelium is very thin.

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Exposing the Cholesterol Myth (5:44)

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Particle Damage

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Neither triglycerides nor cholesterol are elevated by ea?ng saturated fat in general or high cholesterol foods.

Triglycerides are elevated by ea?ng a diet high in Ω6.

High triglycerides

Low HDL cholesterol

Low Intake of Saturated Fat Low intake of saturated fat is a factor in increasing your risk of heart disease.

Your body manufactures 8090% of your cholesterol.

Very liPle of it comes from the diet.

Most people have a gene?cally preset level for the cholesterol in their bodies.

Seek to stay within that range.

If you cut all the cholesterol out of your diet, your body will simply start making more to bring it back up into the range.

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In_lammation in Arterial Walls Damage on the artery wall causes inﬂamma?on and the body responds by recrui?ng cells to ﬁx the problem.

Macrophages clean up the debris •  bacteria •  calcium •  cholesterol

If the cap bursts, the plaque's contents are released and a clot may block the artery  heart aPack.

A ﬁbrous cap grows over the plaque to conceal the inﬂamma?on.

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In_lammation

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Triglycerides are elevated by ea?ng sugar.

Dietary deﬁciency of saturated fats and cholesterol

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Triglycerides  the primary risk factor increasing the chance of having a heart aPack or stroke.

Real Causes

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Coenzyme Q10 a naturally-‐occurring compound found in every cell in the body

plays a key role in producing energy in the mitochondria

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Primary Causes of Heart Attacks and Strokes

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Sta?ns such as Lipitor, Crestor and Zocor, block the ac?on of a chemical in the liver which is necessary for making cholesterol.

It has been a long-‐standing theory that sta?n-‐associated muscle pain is caused, or at least partly contributed by, a reduc?on in CoQ10 levels in muscle mitochondria.

Sta?ns cause the inhibi?on of a pathway which decreases the forma?on of CoQ10 (one of the most important nutrients in the body)

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Heart of the Matter (ABC) (1.32)

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The Problem with Statins

When CoQ10 is depleted it causes the LDL cholesterol to become oxidized.

This sets oﬀ a cascade of events making the LDL cholesterol ‘drill holes’ in the arterial wall causing major inﬂamma?on.

This inﬂamma?on sets the body up for an increased risk of heart aPack or stroke.

The Problem with Statins Cogni?ve loss

Increase cancer risk

Pancrea?c dysfunc?on

Neuropathy

Sexual dysfunc?on

Immune system suppression

Increase cancer risk

Cataracts

Muscle weakness

Kidney failure

Frequent fevers

Ligament and joint pain

Anemia

Acidosis

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Polyneuropathy

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Sta?ns are a class of medicines used to lower blood cholesterol levels.

The Problem with Statins

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Sugar and Heart Disease The focus on cholesterol has been destruc?ve because the real promoters of heart disease are:

Sugar is far more damaging to the heart than fat.

inﬂamma?on oxida?ve damage sugar in the diet stress

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Statins

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Leptin Resistance

What is Leptin? Lep?n is a hormone which plays a key role in regula?ng energy intake and energy expenditure

Lep?n is one of the most important hormones in the body determining health and lifespan.

Acts like a gatekeeper -‐ it surveys and maintains the energy balance in the body, and it regulates hunger.

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Leptin Resistance Video (1.55)

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Sta?n drugs There are The old test have mul?ple nutrients The The demon for good and serious side conven?onal in the diet is which are bad eﬀects and extremely sugar and cholesterol is wisdom on are being fat i s w rong. junk f ood. important f or obsolete. widely heart health. overused.

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Lep?n works in tandem with insulin.

Lep?n resistance, together with insulin resistance, is associated with obesity.

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Cholesterol does not cause health disease  not even a good predictor of it.

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To Summarise

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Lep?n resistance is associated with: high blood pressure

obesity

heart disease

stroke

blood sugar related problems

premature ageing

If a person is trying to lose weight or improve a chronic health condi?on, there is a chance that he / she has lep?n resistance.

As with all hormone issues, lep?n resistance is a complex issue with no singular cause.

High Fructose consump?on can nega?vely impact lep?n levels

Other causes of Leptin Resistance include:  stress levels  simple CHO  sleep  insulin levels  ea?ng

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 exercising

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Many people are lep?n resistant with a mul?tude of health problems as a consequence.

Leptin Resistance

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B12 De_iciency Low Vitamin B12 causes early brain shrinkage and white maPer lesions.

Vegetarian?

Antacids?

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Leptin Resistance

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Poor diet or diges?on?

 excess grain consump?on

Vitamin B12 deﬁciency is caused by pernicious anemia.

Pernicious anemia is caused by a lack of glycoprotein called intrinsic factor.

Without the glycoprotein, which is required for absorp?on of Vitamin B12, a deﬁciency occurs.

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B12 De_iciency When intrinsic factor is secreted by the stomach it binds with B12 and is transported to the small intes?ne for absorp?on.

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B12 De_iciency

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When the absorp?on is unable to occur, a B12 deﬁciency is the result. 581

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When Vitamin B12 is deﬁcient or impaired, the rate of cell division is slowed.

When this slow division occurs, red blood cells are enlarged and are more likely to be destroyed by the immune system.

It is important to eat foods rich in Vitamin B12 or to incorporate supplements of B12 to avoid health problems.

Incon?nence Chronic Fa?gue Weight Loss Shortness of Breath Tingling in Fingers and Toes Forge‰ulness and Confusion Psychosis and Hallucina?ons Tremors Depression Neurological symptoms

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Symptoms of B12 De_iciency

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Neurological Symptoms Neurological symptoms ogen happen ager a prolonged Vitamin B12 deﬁciency and can be confused with other disease such as:

Gullian-‐Barre Syndrome

Mul?ple Sclerosis

Alzheimer's

Parkinson's Disease

Amyotrophic Lateral Sclerosis (ALS)

Burning neuropathic pain can be caused by a low B12 level.

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Neuropathic Pain and B12

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There are several tests that can be performed to diagnose a Vitamin B12 deﬁciency and rule out any other health problems.

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Vitamin B12 is required for the conversion of homocysteine to methionine, which is one of the essen?al amino acids required to synthesize proteins.

Tests for B12 De_iciency

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Stress Consider the global eﬀects of stress on gut health, pain and inﬂamma?on.

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B12 De_iciency

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Stress drives cor?sol levels up and creates a rela?ve DHEA deﬁciency. (DHEA is an adrenal hormone) raised cor?sol related to hypoglycaemia & insulin resistance lack of sleep

Bodily stressors may include:

stressful situa?ons e.g. ?ssue damage, inﬂamma?on, pain

Stress Cortisol and Gut Health Physiological stressors may include: gluten intolerance

lactose fructose or sucrose intolerance

the presence of parasites or pathogens

delayed food sensi?vity

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Stress Cortisol and Gut Health

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mental or emo?onal stress

The average adult makes about 25 mg of DHEA per day with dwindling produc?on as we get older.

DHEA (Dehydroepiandrosterone) Men at all ages have more DHEA than women.

Natural DHEA produc?on is at its highest in the twen?es

A decline in DHEA with the passage of ?me is natural

DHEA is a very powerful precursor to all of major sex hormones.

Stress, Cortisol and Gut Health An elevated Cor?sol to DHEA ra?o will also impact on ﬁrst-‐line immune defense by interfering with the integrity of the body's mucosal linings. The adrenal hormones:

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cor?sol and DHEA systemically modulate the produc?on and turnover of specialized immune cells, immunocytes, which produce the protec?ve secretory

an?bodies par?cularly the primary an?body of defense, secretory IgA (sIgA).

593

590

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DHEA, is a steroid hormone synthesized from cholesterol and secreted by the adrenal glands.

Jacob C et al. J Clin Immunol 2008;28:S56–S61

592

Stress, Cortisol and Gut Health With an elevated cor?sol and low DHEA, the mucosal immune cells are suppressed resul?ng in a low sIgA output.

The gut mucosal surface becomes vulnerable to food an?gens, opportunis?c bacteria, yeast and parasi?c infec?on. Jacob C et al. 2008 ‘Autoimmunity in IgA Deﬁciency: Revisi?ng the Role of IgA as a Silent Housekeeper’ J Clin Immunol 28 (Suppl 1):S56–S61

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DHEA (Dehydroepiandrosterone)

589

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Jacob C et al. J Clin Immunol 2008;28:S56–S61

594

With a chronically heightened HPA axis the body is in a hyper inﬂamed state due to chronically raised cor?sol.

The body’s ability to deal with further physiological stressors such as food intolerance/ sensi?vity or the presence of parasites or pathogens may be compromised. Jacob C et al. 2008 ‘Autoimmunity in IgA Deﬁciency: Revisi?ng the Role of IgA as a Silent Housekeeper’ J Clin Immunol 28 (Suppl 1):S56–S61

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Stress, Cortisol and Gut Health

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Cor?sol Aldosterone 595

596

Over ?me with chronically raised stress levels, the adrenals may not be able to maintain the high levels of cor?sol and adrenal fa?gue will come into play.

Adequate Sleep It can be a gradual process or a crash may be imminent.

Ge•ng adequate rest and sleep is cri?cal to ?ssue repair and pain control.

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597

599

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Chronically raised stress puts increased demand to produce cor?sol at the expense of the steroid hormones, including DHEA and progesterone, and aldosterone.

Avoid Adrenal Burn Out

598

Supplementation Supplementa?on of essen?al nutrients to support adrenal func?on can improve the body’s ability to deal with stress.

In the adrenals, LDL cholesterol is shunted to the mitochondria when needed to make cor?sol.

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Avoid Adrenal Burn Out

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Courtesy of Nick Theideman, Bio Concepts

600

100

Wilson, J, 2010, Adrenal Fa?gue; “The Big Burn Out” A5M, 4th Annual Conference in An?-‐Aging Medicine & Aesthe?c medicine,

Cofactors needed at various stages in the Krebs cycle include Vitamins B1,B2,B3,B5,B6, B12 plus magnesium, calcium and lipoic acid.

601

602

High insulin levels inhibit the levels of enzymes involved in steroid synthesis.

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Ω3 EFA’s Protect against Cortisol

To produce pyruvate by glycolysis we also need vitamins B1, B2, B3, B6, coenzyme A, lipoic acid and magnesium.

Wilson, J, 2010, Adrenal Fa?gue; “The Big Burn Out” A5M, 4th Annual Conference in An?-‐Aging Medicine & Aesthe?c medicine,

Ω3 EFA’s Protect against Cortisol

Impaired steroid hormone ac?vity can result in enhanced produc?on of cor?sol and reduced synthesis of the anabolic steroids DHEA, androstenedione and testosterone

thereby increasing protein ?ssue catabolism and reducing lean-‐body mass.

603 \ Maes, M, 2009, ‘Management of Neuro-‐endocrine and Immune Dysfunc?on in Psychiatry’

docosahexaenoic acid (DHA) Supplementa?on with: eicosapetanoic acid (EPA)

604 Maes, M, 2009, ‘Management of Neuro-‐endocrine and Immune Dysfunc?on in Psychiatry’

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Ω3 EFA’s Protect against Cortisol

Body Biorhythms

has been shown to have protec?ve eﬀects by preven?ng ini?al HPA hyperac?va?on and hippocampal damage from excessive cor?sol.

605 Maes, M, 2009, ‘Management of Neuro-‐endocrine and Immune Dysfunc?on in Psychiatry’

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Vitamin and mineral supplementa?on to support mitochondrial ATP synthesis / energy produc?on should be considered.

Cells under stress can die without adequate nutrients.

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There is a 19 step process from cholesterol to pregnenolone and this eventually converts to cor?sol via progesterone  energy intense process.

Supplementation

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Supplementation

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606

How does sleep eﬀect ?ssue repair?

101

11pm -‐1am

9-‐11 pm 1-‐3 am 7-‐9 pm

3-‐5 am

5-‐7 pm

5-‐7am

The Importance of Quality Sleep Does your client have trouble ge•ng to sleep or lie

Restoring sleep can be a key factor in recovery.

Is you client awake for hours unable to get back to sleep?

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The 24 Hour Body Clock

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3-‐5 pm Do they wake unrefreshed in the morning?

7-‐9 am 1-‐3 pm

9-‐11am

607

608

Is the brain ge•ng what it needs to restore sleep?

Repair does not happen unless quality stage 4 sleep is achieved.

The immune system is heavily dependent on the delicate balance of stress chemicals which can have harmful consequences if it is upset by a lack of sleep.

Sleep Deprivation

Sleep depriva?on exacerbates heart disease and obesity, increases the risk of cancer as well as spoiling produc?vity and leading to accidents.

In a recent study in France, men deprived of sleep were found to have high levels of noradrenaline which has the eﬀect of raising HR & BP as well as inﬂuencing blood sugar.

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609

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Chronic pain pa?ents may have diﬃculty going to sleep or wake at various ?mes through the night.

Sleep Deprivation

610

The Importance of Quality Sleep

According to a recent study in London, powernaps of ½ hour can reverse much of the chemical damage done to the body by a poor night’s sleep.

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The Importance of Sleep is Often Underrated

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11am -‐1pm

They also had low levels of interleukin-‐6, an an?viral protein immune systems disrupted.

611

612

102

Report in The Times, London 12/02/15

Pain Puzzle biorhythms

sleep disturbance of the 24 hour body clock

energe?c balance in the organs

Sleep Melatonin prepares the body for sleep.

GABA maintains non REM sleep by shu•ng down brain ac?vity.

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What nutrient cofactors could be causing neurotransmiPer deﬁciency and aﬀec?ng quality of sleep?

614

Sleep

Sleep ini?a?on is induced by accumula?on of the by-‐ product of cellular metabolism, adenosine, and the inﬂammatory mediator prostaglandin-‐D2.

When the body has been working hard, exercising without rest, or is inﬂamed due to illness or injury, sleep is induced to recover from damage or ?ssue stress.

when you eat

As clinicians, we are trained to look at the biomechanical factors contribu;ng to pain but chronic pain is mul;factorial.

It is important for recovery to examine sleep paPerns closely.

613

615

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nutri?onal deﬁciencies related to diet and lifestyle factors

Is the ?me they wake relevant? Pain suﬀerers ogen wake at ‘Liver ?me’ between 1-‐3 am.

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Napping is not as good as ge•ng a good night’s sleep however a ‘power nap’ has a posi?ve eﬀect which is dispropor?onately great considering the number of minutes slept.

Agernoon naps were more beneﬁcial.

Quality Sleep

Does your client have dream recall? Vitamin B6?

617

616

Practical: Abdominal Diagnosis

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According to the study, Power Naps appeared to wipe out all damage sustained through sleep loss restoring noradrenaline to normal.

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Power Napping

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618

103

Enlarge d Liver

Tender large intesEne

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Abdominal Palpation

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Lunch

the produc?on of free radicals

the ability of the body to counteract or detoxify their harmful eﬀects through neutraliza?on by an?oxidants

Free Radicals

compounds with an unpaired electron

extremely reac?ve

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621

623

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Oxidative Stress Ageing Process

622

Antioxidants

molecules present in cells which donate an electron to the free radicals without becoming destabilized

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Oxidative Stress and the Ageing Process

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620

624

104

Understanding Antioxidants

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625

626

Free Radicals

highly reac?ve, short-‐lived molecules

damage cells and gene?c material (DNA)

73,000 free radical aPacks on DNA every day in a cell

implicated in most health condi?ons

accelerate the ageing process

Environmental polluEon •  smog •  ozone •  NO2

RadiaEon exposure •  sunlight (UV-‐ light) •  X-‐rays

Smoking

10,000,000,000 ,000,000 free radicals per cigarePe!

EaEng & Breathing •  metabolism cycle of mitochondria

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627

Where do Free Radicals come from?

629

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An?oxidants

stop the chain reac?on of free radical forma?on and boost our immune system

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Free Radicals

How Antioxidants Work

628

Antioxidants mi?gate the ageing processes and improve immunity and overall health

cardiovascular func?on

eye health

CNS health

skin health

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Oxidative Stress

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630

105

many an?oxidants work together

important to have a steady supply of dietary an?oxidants

metabolic disease heart and blood vessel disorders atherosclerosis heart failure /aPack

selenium zinc manganese polyphenols

lutein

Causes of Disease 1. Cellular Toxicity

2. Cellular (Nutri?onal) Deﬁciency

lycopene

Biophotonic Scanner

measures current level of an?oxidant status

633

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carotenoids:

632

635

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metallo-‐enzymes (cofactors)

3. Cellular Energy Deﬁciency

cancers chronic fa?gue syndrome

634

Nutrient De_iciency Vitamin deﬁciency syndromes

Nutrient intakes above deﬁciency levels, but below op?mal intakes do not allow for op?mal health.

Most people do not consume op?mal nutrient levels through their diet alone.

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Vitamin C

α & β-‐carotene

gene muta?ons

inﬂammatory diseases

Vitamin E

ﬂavonoids:

neurodegenera?ve diseases

631

Sources of Antioxidants

catechins

Pathophysiological Conditions

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Antioxidant Defense System

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636

106

short-‐term func?onality rather than long-‐term health

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638

Highest Priority

minute-‐to-‐minute and day-‐to-‐day body func?oning circula?on

op?mal blood pressure

diges?on

breathing

consciousness

Lowest Priority those that make for longevity keeping up a strong an?oxidant response

DNA damage repair

minimising glyca?on

minimising inﬂamma?on

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639

641

640

Consequences of Triage The consequences may be completely unno?ced in day-‐to-‐day experience but are likely to show up late in life as: Cardio-‐ cancers

Alzheimer’s

Parkinson’s

diabetes

vascular diseases

other terminal illnesses

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micronutrients are allocated according to triage priori?es

637

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Micronutrient Triage Theory of Ageing

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642

107

completes bone nutri?on

promotes healthy immune func?on

supports normal blood sugar metabolism

protects against DNA damage by free radicals

raises an?oxidant defense

You s?ll need a healthy diet consuming at least nine servings of vegetables & some fruit each day.

Supplementa?on can provide nutri?on insurance

Cellular Toxicity A report by the Environmental Working Group is based on tests of 10 samples of umbilical-‐cord blood taken by the American Red Cross.

≈ 287 contaminants in the blood:

ﬁre

mercury

retardants

pes?cides

Teﬂon chemical PFOA

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643

644

Cellular Toxicity Of the 287 chemicals detected

80 cause cancer in humans or animals

217 toxic to the brain and nervous system

208 cause birth defects or abnormal development

Mitochondria become dysfunc?onal due to nutri?onal deﬁciencies. carni?ne

ribose

CoQ10

acetyl l-‐ carni?ne

alpha-‐lipoic acid

following speciﬁc diet and supplement protocols  energy produc?on can be restored and maintained

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645

Cellular Energy De_iciency

647

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cardiovascular beneﬁts

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addresses nutrient deﬁciencies

Healthy Diet plus Supplementation

646

Glycation AGE’s Glyca?on is the biochemical term for the bonding of sugar molecules to proteins, fats and amino acids.

forms advanced glyca?on end products (AGE’s), which cause protein ﬁbres to become misshapen and inﬂexible.

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The Case for Supplementation

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648

108

According to research on Diabe?c pa?ents, the connec?ve-‐?ssue damage and chronic inﬂamma?on resul?ng from diabe?cs' sustained high blood sugar can lead to debilita?ng condi?ons such as:

cataracts

Alzheimer's

vascular ?ghtening

pancrea?c disease

liver disease

• collagen and elas?n

651

AGE’s When those proteins hook up with renegade sugars, they become discoloured, weak, and less supple The presence of AGE’s also makes the complexion more vulnerable to UV light and cigarePe smoke.

• wrinkles, sagginess, loss of radiance.

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The proteins in the skin most prone to glyca?on are the same ones that make a youthful complexion plump and springy

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AGE’s

650

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649

653

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Glycation

652

When Proteins are Glycated They become less func?onal.

They aPach themselves to similarly damaged proteins and form cross linkages which render them even less func?onal.

They become the source of a drama?c increase in the produc?on of free radicals.

It leads to the destruc?on of ?ssues, damaging fat, other proteins and even DNA.

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Video on Antioxidants & Free Radicals(4)

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654

109

To reduce oxida?ve stress and the ac?on of free radicals harming your brain, you have to reduce the glyca?on of proteins.

The link between oxida?ve stress and sugar can’t be overstated.

High levels of Glycation Cogni?ve decline

Kidney disease

Vascular disease

Diabetes

Premature Ageing

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655

Any protein in the body can be subject to being damaged by glyca?on and can become an AGE.

656

Oxidative Stress and Cognitive Decline LDL is an important carrier protein  vital cholesterol to the brain cells

Only when it becomes oxidised does it wreak havoc on blood vessels.

When proteins are glycated, the number of free radicals formed is increased x 50  loss of cellular func?on and eventually cell death.

When LDL becomes glycated this drama?cally increases its oxida?on.

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657

AGE’s (1.43)

659

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Glyca?on is a normal part of our metabolism but when it is excessive, problems arise

Reduce Oxidative Stress

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Problems with Excess

658

Fatty Liver FaPy liver disease (steatosis) is a build-‐up of excess fat in the liver cells.

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660

110

increased pro-‐inﬂammatory cytokines including TNF-‐a and reac?ve oxida?ve species

chronic inﬂamma?on

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The lipogenic aﬀect of chronic hyper ac?va?on of the HPA axis and cor?sol produc?on is therefore not opposed.

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Fat

Cor?sol McArdle et al, 2013 ‘Mechanisms of obesity-‐induced inﬂamma?on and insulin resistance: insights into the emerging role of nutri?onal strategies’ Nutrigenomics Research Group, UCD Conway Ins?tute, School of Public Health, Physiotherapy and Popula?on Science, University College Dublin, Dublin, Republic of Ireland

665

hyper triglyceridemia

hepa?c insulin resistance

McArdle et al, 2013 ‘Mechanisms of obesity-‐induced inﬂamma?on and insulin resistance: insights into the emerging role of nutri?onal strategies’ Nutrigenomics Research Group, UCD Conway Ins?tute, School of Public Health, Physiotherapy and Popula?on Science, University College Dublin, Dublin, Republic of Ireland

Non-‐Alcoholic Fatty Liver Disease (NAFLD) describes a range of condi?ons caused by a build-‐up of fat within liver cells

It is very common and in many cases is linked to being obese or overweight.

Most people with NAFLD do not develop serious liver problems.

In some people, the build-‐up of fat in the liver can lead to serious liver disease

663

Non-‐Alcoholic Fatty Liver Disease

chronic hyperglycaemia

661

Non-‐Alcoholic Fatty Liver Disease

lipogenesis is enhanced resul?ng in:

Liver Detoxi_ication

The presence of IBS with leakage of larger food par?cles and food an?gens into the submucosal circula?on puts a direct strain on the Liver’s ability to deal with toxins.

Diets high in CHO’s and low in nutrients do not sustain eﬃcient phase 1 and phase 2 detoxiﬁca?on.

Poor liver clearance of toxins can be another reason for increased peripheral pain.

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the inhibitory eﬀect of insulin on hepa?c gluconeogenesis is interrupted

662

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Non-‐Alcoholic Fatty Liver Disease

664

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666

111

Phase 1 and phase 2 occur in the liver; phase 3 is elimina?on.

If phase 1 is out of sync with phase 2,problems occur.

If phase 1 is faster than phase 2 or essen?al nutrients to run phase 2 are deﬁcient, accumula?on of toxic oxida?ve intermediary substances will accumulate.

Ensure essen?al nutrients for both phase 1 and 2 are present.

668

Symptoms of Toxic Build up Headaches Muscle aches and pains Respiratory complaints Chronic Fa?gue Allergies: increased sensi?vity to allergens e.g. perfumes Skin disorders: eczema, rashes Neurological toxicity: •  brain fog •  mood disorders

abnormal

libido menstrua?on

response glucose disregula?on to stress

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669

Endocrine Dysfunction Toxic Build up

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667

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Three phases of Detoxi_ication

670

Genomic Variations

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fer?lity

671

672

112

Alcohol consump?on

Drinking tap water and inadequate hydra?on

Caﬀeine

CigarePe smoking

Drug abuse

Ongoing medica?on use

Exposure to environmental toxins

Lack of exercise

Poor waste clearance-‐ cons?pa?on

Essential Phase 2 Nutrients Selenium

Choline bitartrate Methionine

B6-‐ Pyridoxal-‐5-‐Phosphate

Inositol

B12 -‐Cyanocobalamin

Glutamic acid

Folinic Acid

Magnesium

Molybdenum

Taurine

Manganese

Potassium

Cysteine

Glycine Zinc

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673

Niacin

Magnesium

Zinc

Vitamin C

Vitamins B2, B3, B6, B12

Copper

Folic acid

Phosphatidylcholine & Liver Health The liver’s ability to renew itself and func?on at an op?mal level depends on how well it can make new cells and regenerate.

675

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Diet high in processed foods and nutrient poor

Liver Phase 1 Nutrients

674

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Poor Liver Function Aggravated by:

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676 Kidd, P, 1996, Phospha?dylcholine:A Superior Protectant Against Liver Damage, Alterna?ve Medicine Review

Beneﬁts of supplementa?on with (PC) include: reverse faPy liver

recover from inﬂamma?on

reduce leakage of enzymes from liver ?ssue,

reduce chronic liver damage and cell death

PC & Liver Health Alcohol dissolves the phospholipids so that there are insuﬃcient amounts of PC to metabolize fats.

Fats then accumulate and the parenchymal cells cannot perform their usual func?ons.

The membrane proteins become inac?ve and the mitochondrial func?on is impaired.

677 Kidd, P, 1996, Phospha?dylcholine:A Superior Protectant Against Liver Damage, Alterna?ve Medicine Review

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Phosphatidylcholine (PC) & Liver Health

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678 Kidd, P, 1996, Phospha?dylcholine:A Superior Protectant Against Liver Damage, Alterna?ve Medicine Review

113

In hepatocytes, ALA in both forms have been found to reduce cadmium-‐induced toxicity. 679

680

Bio_lavonoids, Diet, Lifestyle

Nichols, T, Jr. 1997, ‘Alpha-‐Lipoic Acid: Biological Eﬀects and Clinical Implica?ons’ Alterna?ve Medicine Review Berkson, B, 2007. ‘Alpha Lipoic Acid and Liver disease’ ‘Townsend LePer’ The Examiner of Alterna?ve Medicine.

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Nutritional Pain Relief

Quercetin has an?oxidant, an?-‐histamine aﬀects, and inhibits platelet ac?va?ng factor (PAF)

found naturally in blueberries and cranberries

also down regulates NF-‐kappa B, TNFα, prostaglandin E2, series 4 Leukotreines, and histamine

can therefore inhibit inﬂammatory mediators prostaglandin E2, PAF and thromboxane which exacerbate inﬂamma?on

effec?veness can be enhanced by concurrently taking Bromelain, an extract from pineapple which has an?-‐ inflammatory, an?-‐oedematous, an?thrombo?c and fibrinoly?c effects

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681

Quercetin

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It can regenerate CoQ10, Vitamin C and Vitamin E, and NADH via glutathione.

It also has the ability to increase intracellular glutathione and chelate transi?on metals such as mercury, lead and arsenic.

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ALA acts as an an?oxidant in fat and water soluble ?ssues and in it’s reduced form, dihydrolipoic acid(DHLA)

Alpha Lipoic Acid and Liver Health

682

Curcumin Curcumin natural polyphenolic compound

inhibitor of bradykinin

improves an?oxidant ac?vity by increasing levels of superoxide dismutase and glutathione peroxidase

683

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Alpha Lipoic Acid (ALA) and Liver Health

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684 Houston, M. ‘Non-‐pharmacological Treatment of Dyslipidemia’ Health prac??oner’s Guide to An?-‐Aging & Regenera?ve Medicine, 1st Ed. (2010-‐2012) A4M An?-‐Aging Academy of An?-‐aging medicine

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facilitator of phase I and phase II detoxiﬁca?on assis?ng clearance of toxins

an?-‐inﬂammatory and an?-‐infec?ous ac?ons

Diet

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Curcumin

reduce reﬁned carbohydrates

limit starchy carbohydrates

avoid caﬀeine, tea, alcohol, sog drinks

avoid saturated and trans fats

limit animal fats-‐ Ω6 685

686

test for food sensi?vi?es gluten

dairy

ﬁsh

nuts

shell ﬁsh

eggs

soy

salicylates

Diet elimina?on diet

Increase oily ﬁsh consump?on-‐ Ω3 Consume adequate protein and vegetable sources of micronutrient cofactors for ?ssue repair and neurotransmiPer produc?on

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Diet

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Houston, M. ‘Non-‐pharmacological Treatment of Dyslipidemia’ Health prac??oner’s Guide to An?-‐Aging & Regenera?ve Medicine, 1st Ed. (2010-‐2012) A4M An?-‐Aging Academy of An?-‐aging medicine

Take a regular probio?c

AcEvity level: Do you sit all day at work? Sta;c postures s;ﬀen ;ght muscles and joints and reduce elas;city of your blood vessels. Exercise: >30 minutes of moderate exercise daily is recommended plus daily range of movement stretches

Decrease Stress: stress builds cor?sol and heightens the HPA axis

Sleep: if you don’t sleep enough, your body can’t repair and the stress hormone cor?sol is needed to keep going

689

688

The image part with relationship ID rId7 was not found in the file.

Vitamin D mediates cytokine produc?on, lymphocyte and macrophage ac?vity and monocyte matura?on

down regulates inﬂammatory cytokines interleukin IL-‐ 2 and IL-‐12,

suppresses the an?gen producing ability of dendri?c cells and macrophages.

Reduced transport of Vitamin D to the ?ssues would also aﬀect the immune system response.

Vitamin D supplementa?on reduces BP, weight gain and depression in diabe?c women.

A number of studies have associated chronic low Vitamin D levels with elevated triglycerides, dyslipidemia, insulin resistance and obesity.

Gropper, S, Smith, J & Groﬀ, J 2009, Advanced Nutri?on And Human Metabolism, 5thed. Wadsworth, Belmont, Canada p395-‐398

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Lifestyle Factors Vitamin D: Do you work inside all day?

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687

690

The American Diabetes Associa?on 73rd Scien?ﬁc Sessions, Chicago June, 2013. Wlodek, D et al Journ of Theo Bio 2003; 225, 33-‐44

115

When your pH levels are balanced internally your body is full of vitality, increased energy and mental clarity.

Alkalinity To reach and maintain op?mum health, your blood, ﬂuids and delicate ?ssues throughout your body must remain alkaline.

This is in a constant state of ﬂux as most metabolic processes in your body create acidic by-‐products.

Your body is constantly working to maintain a very delicate balance between acid and alkaline.

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692

Dangers of too much Acid When your body is out of balance and becomes too acidic your health is directly aﬀected.

It becomes stressed and suscep?ble to many health issues.

Lack of energy / fa?gue Weight gain Muscle aches and pains Frequent colds and ﬂu Nasal conges?on and excess mucus produc?on Anxiety and irritability

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693

Symptoms of too much Acid

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All life on earth needs to maintain a pH balance for op?mal func?on.

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pH is an important measurable parameter of your body’s health

Alkalinity

694

Acid  In_lammation

Increase in body acidity will increase inﬂamma?on, sog ?ssue degenera?on and bone loss  increase in pain and damage to body ?ssues.

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Acid / Alkaline Balance

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Poor diges?on 695

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Consuming Acidic-‐Forming Foods A food’s acid or alkaline-‐forming tendency in the body has nothing to do with the actual pH of the food itself.

too many processed foods

overcooked meals

lots of animal products

lots of grains

acidic water

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698

It’s about the Residue Lemons are very acidic but the end result ager diges?on and assimila?on is alkaline, so lemons are alkaline-‐forming in the body.

Likewise, meat will test alkaline before diges?on but leaves an acidic residue in the body so, like most animal products, is acid-‐ forming.

Some people have an impaired ability to metabolize acids which the body creates so they may eat a reasonably alkaline diet, yet be extremely acidic.

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Your body creating acids (toxicity and stress)

701

addi?ves like sugar, salt and chemicals

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the modern diet is very acidic

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alkaline

Consuming Acidic-‐Forming Foods

700

Your body creating Acids (toxicity and stress) This arises from the kidney’s inability to clear the acids via the urine correctly.

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acid

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It’s all in the Balance

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The readings half an hour before lunch and dinner should be alkaline.

Your body improperly eliminating acids (mineral depletion) Modern agriculture is designed to grow beau?ful and boun?ful lush vegetables.

Unfortunately this translates to mineral deﬁcient plants as their natural growth cycle will take up phosphate and nitrogen fer?lizers at the expense of minerals.

In today’s world we are all deﬁcient in minerals.

If the body is depleted in minerals it cannot func?on biologically correctly and pH will become acidic.

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705

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If the ﬁrst morning urine is reasonably alkaline you have an issue.

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Mineral Depletion As you are rebalancing an acidic system you should be drinking 2 litres of alkaline mineralized water a day.

While tap water is reasonably neutral it does contain some harmful ingredients. Using an appropriate water ﬁlter to balance the pH is important.

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It should be very acidic pH 56.5.

706

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measure your ﬁrst urine of the day for a week

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acid levels:

Is Your Body Improperly Eliminating Acids? (mineral depletion)

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Your body creating Acids (toxicity and stress) To determine

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708

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Ionised water decreases oxida?on-‐ reduc?on poten?al (ORP).

Afternoon Tea

Osteoporosis is a disease characterised by low bone mass and deteriora?on of bone strength.

Osteoporosis Fragile bones are more prone to fracture.

Adverse lifestyle habits such as smoking, excessive drinking or unhealthy diet from as early as the teenage years will inﬂuence

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Bone Remodeling and Modeling (4.13)

www .thei ntegr ated healt 712 haca dem y.co m.au

711

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Osteoporosis

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709

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The PiMag Waterfall is designed to produce water with added minerals in a pH range of 8.5-‐9.5.

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The water produced by this process is pH adjusted.

Osteoporosis Bones are the reservoir for many minerals esp: calcium

phosphorus

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Water Filtration for Alkalized Water

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The healthy body needs a constant level of calcium in the blood since many organs, especially the heart, muscles, and nerves, depend on calcium.

Peak Bone Mass (PBM) lower bone density in later years. 713

714

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Over ?me, as the mineral reservoir is depleted in the bones, the body ends up with thin, briPle bones.

Pa?ents with chronic inﬂammatory disease could be at high risk for fractures due to bone loss as a consequence of malnutri?on, caused by inﬂamma?on and hormonal change.

Inﬂammatory bowel disease (IBD) is associated with increased prevalence of bone demineraliza?on.

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At a given age, bone mass results from the amount of bone acquired during growth i.e. peak bone mass (PBM) minus the age-‐related bone loss which par?cularly accelerates ager menopause.

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Osteoporosis / PBM

gene?c factors

race

gender

nutrients (calcium, protein, phosphate)

endocrine factors (sex steroids, calcitriol, insulin-‐ like growth factor-‐ I (IGF-‐I))

mechanical forces (physical ac?vity, body weight)

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Regulation of Bone Mass

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When these organs demand calcium, they'll steal it from the mineral storehouse in the bones.

In_lammation and Osteoporosis

exposure to risk factors

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A Balanced Diet Protein Vitamin A Vitamin C Vitamin D Vitamin K Calcium Phosphorous

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Osteoporosis

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Bonjour & Rizzoli 1996, Gilsanz 1998

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The vitamins act as hormones which signal receptors on the osteoblasts and osteoclasts.

Vitamins A & D Vitamin A predominantly promotes ac?va?on of osteoclasts and bone resorp?on

Osteoblasts made from bone marrow, are the cells which form bone.

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Osteoblasts

They synthesize and deposit ﬁbrous proteins into a matrix then organise for mineralisa?on of the matrix with phosphorous and calcium to form bone. 721

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With regard to bone mineralisa?on, Vitamins A and D work antagonis?cally. Vitamin A Vitamin D

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Vitamin A vs Vitamin D

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Vitamins A & D Hence Vitamin D deﬁciency, par?cularly in the presence of excess Vitamin A with subsequent reduced absorp?on of Ca, would compromise the mineralisa?on of bone by the osteoblasts.

Vitamin D promotes the ac?on of osteoblasts and bone mineralisa?on

Calcium is what makes our bones hard and strong.

The calcium level in all parts of our bodies (including the amount of calcium in our bones) is regulated by the parathyroid glands.

That's all the parathyroid glands doregulate calcium throughout the body.

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PHT (Parathyroid Hormone)

Through the secre?on of (PTH), these four small parathyroid glands regulate:

how much calcium is absorbed from our diet

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how much calcium is released into the urine by our kidneys

how much calcium is contained within our nervous system and muscles

and how much calcium is stored in our bones.

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PHT (Parathyroid Hormone)

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It is the excess PTH that is causing this. The result of too much PTH is that bones lose their density and hardness.

Fracture Healing

Physiology of Fracture Healing

Fracture healing involves complex processes of cell and ?ssue prolifera?on and diﬀeren?a?on.

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Fracture Healing Video (3.10)

Fracture healing can be divided into three phases.

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Fracture Healing

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When one (or more) of the parathyroid glands are overac?ve (hyperparathyroidism), our bones release calcium constantly into the blood stream.

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Nearly all of this calcium in our bones is readily available to the rest of the body at the request of the parathyroid glands.

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Phase 1: In_lammatory Phase followed by a cytokine cascade  repair cells to the fracture site

immediately upon fracture, a blood clot formsinﬂammatory cells to the wound area.

cells diﬀeren?ate into specialized cells  osteoblasts & chondroblasts

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PHT (Parathyroid Hormone)

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At this ini?al stage, osteoclast cells dissolve and recycle bone debris.

731

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This sog, new bone substance eventually hardens into a hard callous as the bone weaves together over 6 to 12-‐weeks.

Woven bone is remodeled into stronger lamellar bone by the orchestrated ac?on of both osteoblast bone forma?on cells and osteoclast bone resorp?on cells.

Each stage of the fracture healing process brings with it increased nutri?onal demands.

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Nutritional Demands

734

Energy

The whole process requires a great deal of energy, which is generally supplied through the intake of calories in food.

Healing requires the synthesis of new proteins, which is dependent upon an ample supply of amino acids derived from dietary proteins, zinc and Vitamin B6.

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Protein Synthesis

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In this stage, proteins produced by the osteoblasts and chondroblasts begin to consolidate into what is known as a so[ callous.

At this stage the callous begins to mature and remodel itself.

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Begins about two weeks ager the fracture occurs

Phase 3: Remodeling phase

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Blood Supply

An adequate blood supply is also mandatory for fracture healing, so anything which diminishes blood ﬂow (such as smoking or poor circula?on) slows the healing process.

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Phase 2: Reparative Phase

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There are a number of methods you can employ to reduce your pa?ent’s healing ?me. 1 Marsh, DR and Li, G, 1999, The biology of fracture healing: Op?mising outcome, Bri?sh Medical Bulle?n, 55(4):856-‐869

In trauma?c fractures immediate increase in metabolic demands caloric demand three ?mes that of normal.

An ac?ve adult may require 2,500 calories a day but a bedridden, injured pa?ent with mul?ple fractures may need 6,000 calories per day!

If this demand is not met, the healing process is compromised.

Smith, TK. 1987. Preven?on of complica?ons in orthopedic surgery secondary to nutri?onal deple?on, Clin Ortho and Related Research, 222:91-‐97. Kakar, S and Einhorn, TA. 2004. Importance of nutri?on in fracture healing. In Nutri?on and Bone Health, ed. Holick, MF and Dawson-‐Hughes, B, Totowa, NJ:Humana Press, Inc.

Check Protein Intake Protein malnutri?on or under-‐nutri?on leads to a “rubbery” callous, compared with the rigid calluses of those with adequate or high protein intake.

Studies document the accelera?on of fracture healing with even a modest 10 to 20 gram increase in protein intake.

Among elderly hip fracture pa?ents, poor protein status at the ?me of fracture predicts fracture outcome.

Bonjour, JP, Schurch, MA, and Rizzoli, R. 1996. Nutri?onal aspects of hip fractures, Bone, 18:139S-‐144S; Schurch, MA, Rizzoli, R, Slosman, D, Vadas, L, Vergnaud, P, and Bonjour, JP. 1998. Protein supplements increase serum insulin-‐like growth factor-‐I levels and aPenuate proximal femur bone loss in pa?ents with recent hip fracture, Ann Intern Med, 128(10):801-‐809.

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Check Protein Intake By volume, roughly half of bone is comprised of protein.

When a fracture occurs, the body is called upon to gather protein building blocks together to synthesize a new structural bone protein matrix. Bonjour, JP, Schurch, MA, and Rizzoli, R. 1996. Nutri?onal aspects of hip fractures, Bone, 18:139S-‐144S; Schurch, MA, Rizzoli, R, Slosman, D, Vadas, L, Vergnaud, P, and Bonjour, JP. 1998. Protein supplements increase serum insulin-‐like growth factor-‐I levels and aPenuate proximal femur bone loss in pa?ents with recent hip fracture, Ann Intern Med, 128(10):801-‐809.

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It’s appropriate to increase caloric intake to promote healing.

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739

Adequate Energy

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People who have had a fracture are not ogen told that they can do anything to make their bones heal faster. At most, they’re told to limit the use of the injured bone or limb.

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Also, the trauma of the fracture itself creates a biochemical burst of pro-‐oxidants (free radicals), causing oxida?ve stress that can overwhelm the body’s an?oxidant reserves.

Nutritional Steps to Accelerate Healing

Speci_ic Amino Acids Speciﬁc amino acids of needed include: lysine

arginine

proline

glycine

cys?ne

glutamin e

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Antioxidants

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Lysine helps to:

743

increase the amount of calcium absorbed into the bone matrix

and aid in the regenera?on of ?ssue.

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Sheweita, SA and Khoshhal, KI. 2007. Calcium metabolism and oxida?ve stress in bone fractures: Role of an?oxidants, Current Drug Metabolism, 8:519-‐525.

In_lammation and Healing

Inﬂamma?on is an essen?al component of the healing process in bone  an important part of the cleaning-‐up and rebuilding process.

In fracture healing, increased free-‐radical produc?on can overwhelm the natural an?-‐ oxidant defense mechanisms.

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In_lammation and Healing This inﬂammatory process involves the cyclooxygenase (COX) enzymes COX-‐1 and COX-‐2.

Many standard non-‐steroidal an?-‐inﬂammatory drugs act by inhibi?ng the COX-‐1 and COX-‐2 enzymes which relieves the pain, but also delays healing.

Vitamin C Nourishing the body to reduce inﬂamma?on naturally speeds healing and soothes the inﬂammatory process.

Bioﬂavonoids querci?n

Flavonols

proanthrocydins

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Nourish for Healing

748

Boost Mineral Intake By weight, bone is approx 70% minerals (calcium, phosphorus, magnesium, silicon, zinc, etc.) and fracture healing requires available minerals.

Most people under-‐consume minerals on an everyday basis, so drawing minerals to the healing site can ogen involve a process of Triage.

Ω3 faPy acids Simşek, A, Senköylü, A, Cila, E, Uğurlu, M, Bayar, A, Oztürk, AM, Işikli, S, Muşdal, Y, and Yetkin, H. 2006. Is there a correla?on between severity of trauma and serum trace element levels?, Acta Orthop Traumatol Turc, 40(2):140-‐143. 9 Kakar, S and Einhorn, TA. 2004. Importance of nutri?on in fracture healing, In Nutri?on and Bone Health, ed. Holick, MF and Dawson-‐Hughes, B, Totowa, NJ:Humana Press, Inc.

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These ruptured collagen strands interact with oxygen-‐ yielding oxygen radical metabolites.

These free radicals are associated with inﬂamma?on; further breakdown of bone collagen; and excessive bone turnover.

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This damage occurs as the collagen strands bone are forcefully broken.

Increased Free Radical Production

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When a bone fracture occurs, a large yield of free radicals is generated by the damaged ?ssues.

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Antioxidants repair Oxidative Damage

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Phosphorus Silicon

Many of these func?ons involve cell prolifera?on. Zinc supplementa?on aids in:

callous forma?on

Copper

enhances bone protein produc?on

s?mulates fracture healing

The main minerals in bone are calcium and phosphorus, in the form of calcium hydroxyapa?te crystals.

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Calcium Hydoxyapatite

This compound plays an important role in regula?ng the elas?city and tensile strength of bone.

752

Calcium Fractures can heal normally, independent of dietary calcium as it is drawn from the skeleton for fracture healing.

Ager that, the diet provides the calcium necessary for fracture repair. As calcium absorp?on is dependent on Vitamin D, these nutrients work synergis?cally.

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Calcium

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Calcium

≈ 200 enzymes require zinc for their func?oning

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Zinc

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Phosphorus Most people consume plenty of phosphorus and ogen too much if the diet is high in processed foods.

However, the elderly, calorie restric?ng dieters, and those on low protein diets ogen do not consume enough phosphorus to meet the needs of new bone forma?on. Kakar, S and Einhorn, TA. 2004. Importance of nutri?on in fracture healing, In Nutri?on and Bone Health, ed. Holick, MF and Dawson-‐Hughes, B, Totowa, NJ:Humana Press, Inc. Key JA, Odell RT Failure of excess minerals in diet to accelerate the healing of experimental fractures. J Bone Joint Surg 1955; 37A:37; and Singh LM, Della Rosa RJ, Dumphy JE. Mobiliza?on of calcium in fractured bones in rats. Surg Gynecol Obstet 1963 126:2:243-‐248.

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Speci_ic Key Minerals

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Bioac?ve silicon enhances the eﬀects of calcium and Vitamin D3 on new bone forma?on.

Vitamins for Bone Healing While protein and minerals may be the building blocks, vitamins are the catalysts for many biochemical reac?ons and are equally important.

Yilmaz, C, Erdemli, E, Selek, H, Kinik, H, Arikan, M, and Erdemli, B. 2001. The contribu?on of vitamin C to healing of experimental fractures, Archives of Orthopaedic and Trauma Surgery, 121(7):426-‐428. Alcantara-‐Martos, T, Delgado-‐Mar?nez, D, Vega, MV, Carrascal, MT, and Munuera-‐Mar?nez, L. 2007. Eﬀect of vitamin C on fracture healing in elderly Osteogenic Disorder Shionogi rats, J Bone Joint Surg Br, 89-‐B(3):402-‐407.

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In severe Vitamin C deﬁciency, collagen becomes too unstable to func?on properly  skin lesions and fragile blood vessels with eventual bleeding from all mucous membranes.

Simşek, A, Senköylü, A, Cila, E, Uğurlu, M, Bayar, A, Oztürk, AM, Işikli, S, Muşdal, Y, and Yetkin, H. 2006. Is there a correla?on between severity of trauma and serum trace element levels?, Acta Orthop Traumatol Turc, 40(2):140-‐143.

757

In fracture healing, we can clearly iden?fy the vital roles of several vitamins including Vitamin C, Vitamin D, and Vitamin K as well as the energy-‐producing B vitamins, which should all be taken in therapeu?c doses.

Vitamin C De_iciency and Bones

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The body’s demand for both copper and zinc rises according to the severity of the trauma.

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Spector, TD, et al. 2005. Eﬀect on bone turnover and BMD in low dose oral silicon as an adjunct to calcium/vitamin D3 in a randomized placebo-‐controlled trial. Abstract from the ASBMR 27th Annual Mee?ng, Nashville, TN.

Copper aids in the forma?on of bone collagen and is important to the healing process.

Vitamin C Essen?al for proper synthesis of the bone collagen protein matrix.

It is one of the most important an?oxidants and an?-‐inﬂammatory nutrients. Yilmaz, C, Erdemli, E, Selek, H, Kinik, H, Arikan, M, and Erdemli, B. 2001. The contribu?on of vitamin C to healing of experimental fractures, Archives of Orthopaedic and Trauma Surgery, 121(7):426-‐428. Alcantara-‐Martos, T, Delgado-‐Mar?nez, D, Vega, MV, Carrascal, MT, and Munuera-‐Mar?nez, L. 2007. Eﬀect of vitamin C on fracture healing in elderly Osteogenic Disorder Shionogi rats, J Bone Joint Surg Br, 89-‐B(3):402-‐407.

Vitamin D Vitamin D is the primary regulator of Ca absorp?on and without adequate Vitamin D Ca blood level drops making less calcium available for fracture healing.

Vitamin D, in conjunc?on with Vitamin K, s?mulates the transforma?on of fracture site stem cells to bone building osteoblasts.

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Bioac?ve silicon (silica) plays an important role in bone collagen synthesis.

Copper

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Silicon

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Overall, Vitamin D is central to fracture healing and Vitamin D status has been shown to be an independent predicator of func?onal recovery ager hip fracture.

Di Monaco, M, Vallero, F, Di Monaco, R, Mau?no, F, and Cavanna, A. 2005. Serum levels of 25-‐hydroxyvitamin D and func?onal recovery ager hip fracture, Arch Phys Med Rehabil, 86(1):64-‐68.

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Vitamin B6 modulates the eﬀects of Vitamin K on bone through complex biochemical pathways.

Reynolds, TM. 1998. Vitamin B6 deﬁciency may also be important, Clin Chem, 44:2555-‐2556.

Vitamin K Vitamin K is sequestered to the site of fracture markedly depressed circula?ng levels of Vitamin K in fracture pa?ents.

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Animals deﬁcient in this vitamin, fracture more frequently and experience reduced fracture healing.

Vitamin K Vitamin K is an essen?al part of the biochemical processes that bind calcium to bone and it is required for proper forma?on of the osteocalcin bone protein.

In addi?on, Vitamin K helps conserve calcium by reducing the loss of calcium in the urine. 763

764 Knapen, MHJ, Hamulyák, K, and Vermeer, C. 1989. The eﬀect of vitamin K supplementa?on on circula?ng osteocalcin (bone Gla protein) and urinary calcium excre?on, Ann Inter Med, 111:1001-‐1005.

Anti-‐in_lammatory nutrients help reduce pain Where there is pain, there is inﬂamma?on a product of the body’s ac?on to tear down, recycle, and repair damaged ?ssue.

The ?me taken for the Vitamin K blood level to return to normal appears to be inﬂuenced by the severity of the fracture. 765

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Vitamin B6 is linked to fracture healing.

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Vitamin B6

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For fracture healing, it is ideal to use nutrients which are both an?-‐ inﬂammatory and nourishing to new bone growth.

Anti-‐in_lammatory nutrients help reduce pain Useful an?-‐ inﬂammatory nutrients include: Vitamin C,

767

querce?n

other ﬂavonoids

Ω3 faPy acids

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Anti-‐in_lammatory nutrients help reduce pain

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Knapen, MHJ, Hamulyák, K, and Vermeer, C. 1989. The eﬀect of vitamin K supplementa?on on circula?ng osteocalcin (bone Gla protein) and urinary calcium excre?on, Ann Inter Med, 111:1001-‐1005.

proteoly?c enzymes such as bromelain and trypsin

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Arthritis Arthri?s is an umbrella term for more than 100 medical condi?ons which aﬀect the musculoskeletal system, speciﬁcally joints.

deformi?es

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This can result in:

instability

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Jamdar, S, Rao, B, Netke, S, Roomi, MW, Ivanov, V, Niedzwiecki, A, and Rath, M. 2004. Reduc?on in ?bial shag fracture healing ?me with essen?al nutrient supplementa?on containing ascorbic acid, lysine, and proline, LePer to the Editor, J Alter and Comp Med, 10(6), 915-‐916. FrassePo, L, et al. 2001. Diet, evolu?on and aging, Eur J Nutr 40:200-‐213. Sheweita, SA and Khoshhal, KI. 2007. Calcium metabolism and oxida?ve stress in bone fractures: Role of an?oxidants, Current Drug Metabolism, 8:519-‐525.

Arthritis-‐Related Problems Arthri?s-‐related problems include: pain

s?ﬀness

inﬂamma?on

damage to joint car?lage

771

Arthritis-‐Related Problems

joint weakness

These growth hormones are among the most important biochemical forces encouraging fracture repair and new bone forma?on.

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Such a ‘base-‐forming ea?ng program’ has been shown to increase growth hormones and growth factors such as IGF insulin-‐ like growth factor.

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damage to surrounding structures

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Following an alkaline diet has been shown to create a health-‐promo?ng internal biochemical environment which conserves bone building minerals and proteins.

Alkaline State

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Arthritis Pain Car?lage destruc?on in Osteoarthri?s is the result of car?lage inﬂamma?on, not just wear and tear.

Studies have shown a signiﬁcant reduc?on in the pain and swelling of arthri?s with dietary changes and exercise.

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Alkaline State

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With all forms of arthri?s we need to consider anything that causes systemic inﬂamma?on.

CARDIOVASCULAR DISEASE

INFLAMMATION

DIABETES

ALZHEIMER’S DISEASE

CHRONIC PAIN

ARTHRITIS AUTOIMMUNE DISEASE

Is Arthritis in our young related to sugars? The NSW study found 50% of children between 5-‐12 years drank more than 2 sugary drinks per day.

A recent Australian Ins?tute of Health and Welfare study performed over 10 years found a threefold increase in children being hospitalised with arthri?s.

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Arthritis facts Obesity is a signiﬁcant risk factor for both the development and progression of knee OA and also to a lesser degree hip OA.

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NEUROLOGICAL DISEASES

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PULMONARY DISEASE

CANCER

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Arthritis

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Arthritis Facts

Arthri?s is the major cause of disability and chronic pain in Australia, with 3.85million Australians aﬀected at a cost to the economy of more than $23.9 billion each year.

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>50% of people over the age of 65 years have radiological evidence of OA, with approximately 10% of men and 18% of women suﬀering symptoma?c OA.

Rheumatoid Arthritis Chronic infec?on from viruses, bacteria and super an?gens found in synovial ﬂuid in RA pa?ents

Autoimmune disease

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Rheumatoid Arthritis Principals of treatment: reduce inﬂamma?on and pain

EFA balance

support immune health

reduce microbial load, Gut dysbiosus / SIBO?

source areas of immune hyperac?va?on

support diges?on and inves?gate food intolerances

op?mise detoxiﬁca?on pathways

support mitochondria

Java et al Interac?on between rheumatoid arthri?s and infec?ons. Infec?on and Autoimmunity, Elselvier, 2004: 729-‐740

The Arachidonic Cascade Poor regulatory eﬀect of the arachidonic acid cascade

Increased inﬂammatory ac?vity/ Immune system hyper-‐ reac?vity

Hyper coagula?on states

Impaired lipid transport

Impaired hormonal & neuronal ac?vity

783

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Arthritis Facts

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18/02/15

784

Eat high quality protein > 0.8gm/kg per day

Increase consump?on of oily ﬁsh ≈ 3 to 4 meals/week

Eat Complex CHO’s  low GI foods reduce insulin response

Diet Tips to reduce In_lammation and Improve Healing Avoid reac?ve foods

Drink 2 litres of ﬁltered water daily,

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Diet Tips to Reduce In_lammation and Improve Healing

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Simopoulos, A, 2002 ‘Omega-‐3 FaPy Acids in Inﬂamma?on and Autoimmune Diseases.’ J Am Coll Nutrit, 21(6):495–505

NOT tea, coﬀee, alcohol or sog drinks 785

786

131

Take a probio?c daily to restore intes?nal balance

Increase vegetables and fruit to supply an?oxidants (ﬂavonoids & carotenoids), and alkalize your body

Take quality ﬁsh oil or krill oil (Ω3)

potently preven?ve of chronic disease

788

Natural Pain Relief

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Helps normalize glucose, insulin, and lep?n levels by op?mizing insulin and lep?n receptor sensi?vity

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787

Exercise

Exercise promotes naturally occurring opioids.

op?misies overall health including mental health

Ω3 fats Vegetarian sources only weakly convert to the ac?ve formﬂaxseed oil, walnuts.

QuerceEn 600-‐1000 mg/day RuEn / Bromelain / Curcumin

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789

Natural Pain Relief

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Add soluble and insoluble ﬁbre to feed “friendly” bacteria

Diet Tips to Reduce In_lammation and Improve Healing

791

790

Different Diets

Low GI

Ketogenic

Gluten-‐ Free

Alkalising

Low Fodmap

Atkin’s

Liver Detox

Mediterranean

Fructose Intoleranc e Elimina?on

High Protein

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Diet tips to Reduce In_lammation and Improve Healing

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18/02/15

792

132

rich in an?oxidants

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low in reﬁned carbohydrates

Group Examination

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793

Case Studies

Case Study 2: Female 45 years Headache Headach Headache Head

High sensi?vity to touch

Ache/ shoot Ac pain

Nausea

Cons?pa?on

Ach Ache e

Disturbed sleep

Low energy

Poor mo?va?on

Scaly skin par?cularly on the legs

Ache Calf C spasms

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795

794

Case Study 2: Female 45 years Head Headache Headache Right sided headache

Ache/ Ac shoot pain

Right sided neck and shoulder pain

Ache Ache Low back ache

Bilateral outside thigh and leg pain

Ache

Calf spasms C

Morning calf cramps

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higher in Ω3 fats

796

Case Study 3: Female 43 years old 5 g 6” tall, 140kg

2 year history constant (L) sided neck to shoulder pain and sub-‐occipital ache

Daily occipito-‐frontal headaches

Ogen wakes with headache

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The Mediterranean Diet

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18/02/15

Low back ache

797

133

R/O gallbladder 10 years previous

Hysterectomy 10 years previous

s?ll has her ovaries

MBA age 14, landed on her coccyx and hit her head

Took Celebrex many years

Extreme sensi?vity to light palpa?on buPocks,

en?re neck and back, over (L) infraspinatus

Unable to perform a spinal palpa?on exam

Gastrointes?nal symptoms Stomach bloat and diarrhea ager ea?ng McDonald’s and milk coﬀee

Drink 1 can of Coke daily

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Pain on (L) neck rota?on, and eleva?on of (L) arm above 90 degrees

Reﬂux ager taking ﬁsh oil

High sugar foods increase her headache

Currently takes panadeineforte daily, panadol-‐osteo, nurofen

Examination

History

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Case Study 3-‐History

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18/02/15

Rotator cuﬀ tests nega?ve

134

theintegratedhealthacademy.com.au Please rate each of the following symptoms according to your recent health status: 0 1 2

Never or almost never have the symptom Occasionally have it, effect is not severe Occasionally have it, effect is severe

3 4

EARS

Frequently have it, effect is not severe Frequently have it, effect is severe

NOSE

DIGESTIVE TRACT

EYES

Stuffy Nose or nasal discharge Sinus congestion/Sinus Infection Hay Fever or sneezing attacks Postnasal drip or excessive mucus production TOTAL MOUTH/THROAT

Watery or itchy eyes ___ Swollen, red or sticky eyelids ___ Bags or dark circles under eyes ___ Blurred or tunnel vision or visual disturbance ___ (Does not include near or farsightedness) ___

Chronic coughing or clearing of throat Frequent gagging or difficulty swallowing Sore throat, hoarseness or loss of voice Swollen or discoloured tongue, gums or lips Mouth ulcers or sore gums

Itchy Ears Earache/ear infections Hearing Loss/Blocked Ears Ringing/Buzzing Ears

___ ___ ___ ___

TOTAL

___ ___ ___ ___

___ ___ ___ ___ ___

___ ___

___ ___ ___

TOTAL

___ ___ ___ ___ ___ ___ ___

Mood swings Anxiety, fear or nervousness Anger, irritability or aggressiveness Depression Hyperactivity or restlessness

___ ___ ___ ___ ___

TOTAL ENERGY/ACTIVITY

Pain or aches in the joints or arthritis Pain or aches in muscles Stiffness or limitation of movement

___ ___ ___

Fatigue, sluggishness or lethargy Apathy or loss of motivation Feeling of weakness or tiredness

___ ___ ___

___

TOTAL

APPETITE/EATING BEHAVIOUR

TOTAL

___ ___ ___ ___ ___

EMOTIONS/FEELINGS

JOINTS/MUSCLES

Irregular or skipped heartbeat Rapid or pounding heartbeat Chest Pain

Acne Hives, rashes or dry skin Hair Loss Flushing or hot flushes Excessive Sweating

___

HEAD Headaches Faintness/light headedness Dizziness or vertigo Insomnia or sleep disturbance

Poor memory Confusion, poor comprehension Poor concentration Poor physical co-ordination Difficulty in making decisions Stuttering, stammering or slurred speech Learning disabilities

___ ___ ___ ___ ___

TOTAL

HEART

Recurrent/ chronic bronchitis Asthma – wheezing or coughing spasms Shortness of breath or difficulty breathing Chest congestion or productive chest cough

Indigestion or abdominal discomfort/pain Abdominal bloating – episodic or recurrent Episodic nausea or vomiting Flatulence – burping or passing gas Heartburn – episodic or recurrent TOTAL MIND/COGNITION

TOTAL

LUNGS

SKIN

___ ___ ___ ___

TOTAL

OTHER

Loss of appetite Food cravings Binge eating, drinking or compulsive eating Excessive weight or weight gain

___ ___ ___ ___

GRAND TOTAL POINTS

Recent illness or recurrence of illness Underweight or rapid weight loss Fluid or water retention Frequent or urgent urination Genital itch or discharge

TOTAL

SIGNATURE ........................................................................... DATE .....................................................................................

___ ___ ___ ___ ___ TOTAL

TOTAL POINTS

____

Measuring*Skinfolds* To#work#out#a#patientâ&#x20AC;&#x2122;s#body#composition#you#will#need#to#measure#4#skin#folds:# 1) mid;triceps,## 2) mid;biceps,## 3) subscapular#and## 4) suprailiac,# Record#each#measurement.### Take#the#measurement#twice#~## if#there#is#a#5mm#difference#between#the#2#readings#at#any#one#site#do#a#third# measurement,#and#a#fourth#if#necessary,#until#you#have#two#measurements# within#5mm.#Average#the#two#closest#readings#for#each#site.### # Analysis*of*body*composition* Information#needed:# 1) The#four#skinfold#measurements#as#discussed#above.# 2) The#weight#of#the#patient#in#kilograms.# 3) The#age#of#the#patient# 4) The#recommended#body;fat#percentage#for#that#age:# Males* Males* Females* Females* <40* <40* <40*yrs* >40*yrs* yrs* yrs* 20%# 25%# 15%# 20%# # * Calculations:* 1. Sum#of#the#skinfolds,#add#the#four#measurements#together:# ## Triceps#+#Biceps#+#Subscapular#+#Suprailiac#=#Total#(mm)# 2. To#determine#the#percentage#of#body#fat#use#the#following#tables:## Table#A#for#females#and#Table#B#for#males.### 3. Use#the#left#hand#column#to#find#the#number#closest#to#the#skin#fold# total.##Match#this#number#up#with#the#appropriate#age#group,#and#that#is# the#body#fat#percentage.# 4. To#work#out#fat#weight#use#the#following#calculation:#

Body#fat#weight#=## Percent#Fat#x#Body#weight# 100# 5. To#work#out#the#patients#ideal#weight#use#the#following#calculation:# # Target#weight##=##100#x#(Body#weight#–#fat#weight)# (100#–#average#%#fat#for#age)# # 6##Measurement#of#lean#weight# ### ####Total#weight;#fat#weight#=#Lean#body#mass#

# # Example*measurement* Female*age*45*years* The#average#skin#fold#measurements:# Mid#triceps;#24mm# Mid#biceps;#14mm# Suprascapular;#38mm# Supra#iliac;#28mm#########Added#total=#104# # According#to#the#table#provided,#her#body#fat#percentage#is#40.4# # Body#fat#weight#=## Percent#Fat#x#Body#weight# # 100# # ########################Body#fat#weight#=#40.4#x#74# ##########################################################100# ###################################################=#29.89#kg# # Target#weight##=##100#x#(Body#weight#–#fat#weight)# (100#–#average#%#fat#for#age)# # # #########################Target#weight#=#100x#(74;#29.89)# ########################################################(100;25)# ################################################=#58.8#kg# #

# Her#lean#body#mass# # Total#weight;fat#weight#=#74#;#29.89# ###########################################=#44.11kg# ## The#following#formula#may#be#used# For#men:#LBM#=#(0.32810#*#W)#+#(0.33929#*#H)#;#29.5336# For#women:#LBM#=#(#0.29569#*#W)#+#(0.41813#*#H)#;#43.2933# This#is#based#on#an#average#and#is#not#accurate#for#the#individual.# #

BODY FAT PERCENTAGE: TABLE A - FEMALES FATFOLDS 16-29 years 30-39 years 40-49 years 50-70 years 15 10.5 20 14.1 17 19.8 21.4 25 16.8 19.4 22.2 24 30 19.5 21.8 24.5 26.6 35 21.5 23.7 26.4 28.5 40 23.4 25.5 28.2 30.3 45 25 26.9 29.6 31.9 50 26.5 28.2 31 33.4 55 27.8 29.4 32.1 34.6 60 29.1 30.6 33.2 35.7 65 30.2 31.6 34.1 36.7 70 31.2 32.5 35 37.7 75 32.2 33.4 35.9 38.7 80 33.1 34.3 36.7 39.6 85 34 35.1 37.5 40.4 90 34.8 35.8 38.3 41.2 95 35.6 36.5 39 41.9 100 36.4 37.2 39.7 42.6 105 37.1 37.9 40.4 43.3 110 37.8 38.6 41 43.9 115 38.4 39.1 41.5 44.5 120 39 39.6 42 45.1 125 39.6 40.1 42.5 45.7 130 40.2 40.6 43 46.2 135 40.8 41.1 43.5 46.7 140 41.3 41.6 44 47.2 145 41.8 42.1 44.5 47.7 150 42.3 42.6 45 48.2 155 42.8 43.1 45.4 48.7 160 43.3 43.6 45.8 49.2 165 43.7 44 46.2 49.6 170 44.1 44.4 46.6 50 175 44.8 47 50.4 180 45.2 47.4 50.8 185 45.6 47.8 51.2 190 45.9 48.2 51.6 195 46.2 48.5 52 200 46.5 48.8 52.4 205 49.1 52.7 210 49.4 53 (From Durnin, J.V.G.A. and J. Wormersley, 1974, British Journal of Nutrition, Vol. 32, pp.77-97).

BODY FAT PERCENTAGE: TABLE B - MALES FATFOLDS 17-29 years 30-39 years 40-49 years 50-70 years 15 4.8 20 8.1 12.2 12.2 12.6 25 10.5 14.2 15 15.6 30 12.9 16.2 17.7 18.6 35 14.7 17.7 19.6 20.8 40 16.4 19.2 21.4 22.9 45 17.7 20.4 23 24.7 50 19 21.5 24.6 26.5 55 20.1 22.5 25.9 27.9 60 21.2 23.5 27.1 29.2 65 22.2 24.3 28.2 30.4 70 23.1 25.1 29.3 31.6 75 24 25.9 30.3 32.7 80 24.8 26.6 31.2 33.8 85 25.5 27.2 32.1 34.8 90 26.2 27.8 33 35.8 95 26.9 28.4 33.7 36.6 100 27.6 29 34.4 37.4 105 28.2 29.6 35.1 38.2 110 28.8 30.1 35.8 39 115 29.4 30.6 36.4 39.7 120 30 31.1 37 40.4 125 30.5 31.5 37.6 41.1 130 31 31.9 38.2 41.8 135 31.5 32.3 38.7 42.4 140 32 32.7 39.2 43 145 32.5 33.1 39.7 43.6 150 32.9 33.5 40.2 44.1 155 33.3 33.9 40.7 44.6 160 33.7 34.3 41.2 45.1 165 34.1 34.6 41.6 45.6 170 34.5 34.8 42 46.1 175 34.9 180 35.3 185 35.6 190 35.9 (From Durnin, J.V.G.A. and J. Wormersley, 1974, British Journal of Nutrition, Vol. 32, pp.77-97).

# 7 Body Mass Chart.indd 1

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# 7 Body Mass Chart.indd 2

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Measuring Skinfolds To work out a patient’s body composition you will need to measure 4 skin folds: 1) mid-triceps, 2) mid-biceps, 3) subscapular and 4) suprailiac, Record each measurement. Take the measurement twice ~ if there is a 5mm difference between the 2 readings at any one site do a third measurement, and a fourth if necessary, until you have two measurements within 5mm. Average the two closest readings for each site. Analysis of body composition Information needed: 1) The four skinfold measurements as discussed above. 2) The weight of the patient in kilograms. 3) The age of the patient 4) The recommended body-fat percentage for that age: Females <40 yrs 20%

Females >40 yrs 25%

Males <40 yrs 15%

Males <40 yrs 20%

Calculations: 1. Sum of the skinfolds, add the four measurements together: Triceps + Biceps + Subscapular + Suprailiac = Total (mm) 2. To determine the percentage of body fat use the following tables: Table A for females and Table B for males. 3. Use the left hand column to find the number closest to the skin fold total. Match this number up with the appropriate age group, and that is the body fat percentage. 4. To work out fat weight use the following calculation: Body fat weight = Percent Fat x Body weight 100 5. To work out the patients ideal weight use the following calculation: Target weight = 100 x (Body weight – fat weight) (100 – average % fat for age)

Deficiency Symptoms and Signs

16/05/14 4:01 PM

This page has been printed from the www.stewartnutrition.co.uk web site.

Deficiency Symptoms and Signs Symptom or Sign

Possible Nutritional Deficiency

Other Possible Causes

General Symptoms and Appearance Fatigue

Protein-energy, iron, magnesium, potassium, vitamins B1, B12 and other B vitamins and vitamin C

Many physical illnesses including hypothyroidism, cardiac failure, anaemia, chronic fatigue syndrome and depression

Loss of appetite

Zinc

Many chronic illnesses

Pica eating non-nutritive substances

General malnutrition and possibly iron, calcium, zinc, vitamins B1 – thiamine, B3 – niacin, C and D

Normal in infants under 2 years of age, pregnancy especially in young women, mental illness

Loss of taste

Zinc

Common cold, many nasal disorders

Cold intolerance

Iron

Hypothyroidism, anaemia and reduced cardiac output

Pale appearance due to anaemia

Iron, folate and vitamin B12

Excessive bleeding and haematological disorders

Carotenoderma – yellow Protein-energy and zinc discolouration of the skin noticeable on the face and trunk

Dietary carotenoid excess especially in women, hypothyroidism

Diffuse hyperpigmentation

Protein-energy

Addison’s disease and haemochromatosis

Muscle wasting e.g. clothes appear too big, loss of limb musculature

Protein-energy

Loss of height and excessive curvature of the spine

Calcium and vitamin D

Increasing age and disease- related osteoporosis

Itchy skin – pruritus

Iron

Many skin diseases, liver disease

Dry skin

Essential Fatty Acids or multiple nutritional deficiencies

Old age, skin conditions e.g. eczema

Skin

Red scaly skin in light-exposed areas Vitamin B3

Excessive sun-exposure in red/fair haired individuals light-exposed areas

Excessive bruising

Old age, trauma and blood disorders

Vitamin C

Haemorrhage or redness around hair Vitamin C follicles Bleeding into a joint or other unusual Vitamin C bleeding

Various blood disorders

Plugging of hair follicles with keratin Vitamin C or coiled hairs Fine downy hair on torso – lanugo

Protein-energy. Typical of Persistent anorexia nervosa

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Deficiency Symptoms and Signs

16/05/14 4:01 PM

Mouth Sore tongue

Iron, vitamin B12, B2, B3 and possibly other B vitamins

Excessively hot drinks and oral disease

Vitamin B2 – riboflavin

Excessive exposure to cold or windy weather

Cracking at the corners of the mouth

Iron, vitamin B2 – riboflavin possibly other B vitamins

Poorly fitting dentures, eczema infection with candida albicans

Recurrent mouth ulcers

Iron, vitamin B12, folate and possibly other B vitamins

Coeliac disease, Crohn’s disease recurrent herpes and oral disease

Enlarged veins under the tongue with micro-haemorrhages

Vitamin C

Smoking and old age

Smooth, shinny and sore tongue: atrophic glossitis

Iron, vitamin B12 and folate

Cracking and peeling of the lips

skin on

Head, Face and Neck Scalp hair loss

Iron

Any scalp disease, alopecia from other causes

Dandruff

Essential fatty acids and biotin

Fungal infection of scalp

Redness at the sides of the nose

Vitamin B2 –riboflavin, vitamin B6 and zinc

Seborrhoeic dermatitis

Redness or cracking at the outer angle of the eyes

Vitamins B2 or B6

Goitre

Iodine deficiency is likely if goitre is present in > 20% of population – endemic goitre

Adolescence, pregnancy and various forms of thyroid disease

Nails - brittle or flaking

Iron acids

Poor circulation and old age

Nails - upturned or spoon-shaped nails

Iron

Hands and Nails and possibly essential fatty

Carotenoderma – yellow Protein-energy and zinc discolouration of the skin noticeable on the palms

Psoriasis or other diseases of the nail bed Dietary carotenoid excess especially in women, hypothyroidism

Musculo-skeletal Muscle pains and cramps

Magnesium, potassium, sodium, vitamin B1 and vitamin D if there is hypocalcaemia

Muscle or neurological disease, polymyalgia rheumatica and hypocalcaemia

Calf muscle pain after minimal exercise

Vitamin B1 – thiamine

Torn muscle, peripheral vascular disease and myopathy

Excessive calf muscle tenderness

Vitamin B1- thiamine

Torn muscle, thrombosis

Walking with a waddling gait

Vitamin D and resultant myopathy

Osteoarthritis of the hips or disease of the hip-girdle muscles

Difficulty getting up from a low chair Vitamin D and resultant myopathy or climbing the stairs or weakness of shoulder muscles

Arthritis of the hips or knees, diseases of the nerves or muscles

Bowed legs

Vitamin D - rickets in childhood

Paget’s disease and syphilis

Twitching of facial muscles when tapping on the facial nerve in front of the ear: Chvostek’s sign

Calcium and vitamin D if Hypocalcaemia for other reasons e.g. hypocalcaemia or severe magnesium hypoparathyroidism deficiency

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Deficiency Symptoms and Signs

16/05/14 4:01 PM

Eyes Poor night vision

Zinc, vitamin A and possibly vitamin Retinal disease B2 - riboflavin

Conjunctival dryness

Vitamin A

Old age and Sjogren’s syndrome

Diarrhoea

Vitamin B3

Irritable bowel syndrome, malabsorption, infective diarrhoea and many other causes

Constipation

Dehydration, fibre, potassium, magnesium and folate

Irritable bowel syndrome, diverticulosis, cancer of the colon

Restless legs

Iron or folate

Various neurological disorders, pregnancy, rheumatoid arthritis, and renal failure

Burning feet syndrome

Vitamin B2 –riboflavin

Early peripheral neuropathy

Loss of balance when standing upright with feet together and the eyes closed: Romberg’s test

Vitamin B12 and possibly vitamin B3 Many neurological disorders affecting the cerebellum, spinal chord or peripheral nerves

Loss of vibration sensation in the lower limbs

Vitamin B12 and possibly vitamin B3 Increasing age and peripheral neuropathy

Gastrointestinal

Neurological

Peripheral neuropathy – numbness, Vitamins B1, B12 and possibly B3, Diabetes and many other causes tingling, disordered sensation, pain B6 and folate and very rarely copper and or weakness in the hands or feet (following gastrointestinal surgery or excess zinc ingestion). Relative lack of essential fatty acids. Unsteady movement or walking (cerebellar ataxia)

Vitamin B1, vitamin E and Coenzyme Q10

Alcohol, hypothyroidism and many neurological and inherited disorders

Mental State Depression

Vitamins C, B1, B3, B6, B12, folate, Mental illness, stress and as a biotin and possibly the essential fatty consequence of physical illness acids

Irritability

Folate

Alcoholism, deprcssion and personality disorder

Poor concentration

Iron, vitamins B1, B12, folate and possibly essential fatty acids

Depression, stress, lack of sleep, alcohol, dementia, anaemia, hypothyroidism and many other diseases

Heart failure

Vitamin B1 – thiamin and any deficiency causing anaemia

Coronary, valvular and myocardial disease

Palpitations

Potassium and magnesium and any deficiency causing anaemia

Coronary, valvular and myocardial disease

Cardio-vascular

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Underpinning Research (A Practical Guide to Nutrition for Allied Health Practitioners) Aydin H, Mutlu N, Akbas N, 2011, ‘Treatment of a major depression episode suppresses markers of bone turnover in premenopausal women.’ J Psychiatr Res. Vol 45(10):1316-20 Berkson, B, Alpha Lipoic Acid and Liver disease, ‘Townsend Letter’ The Examiner of Alternative Medicine, viewed 28/01.2013 www.townsendletter.com/Dec2007/alphalipo1207.htm Best, B, ‘Does Excess Protein Cause Kidney Damage?’ viewed 16 December 2008, www.benbest.com/health/kidney.html Bohl, C & Volpe, S, 2002, Magnesium and Exercise, Critical Review Food Science Nutrition, Vol 42(6):p533-63 Bonjour, J, 2005, ‘Dietary Protein: An Essential Nutrient For Bone Health’, Journal of the American College of Nutrition, Vol 24, No 90006, 526S-536S. Bottiglieri,T., Laundry, M., Crellin, R., Toone, B, Carney, M, Reynolds, E, 2000, ‘Homocysteine, folate, methylation, and monoamine metabolism in depression’. Journal of Neurosurgery Psychiatry, Vol 69; 228-232 Braverman, E & Bajaj, A. ‘Cognitive Diseases and Impairments: Part 1’ Health Practitioner’s Guide to Anti-Aging & Regenerative st Medicine, 1 Ed. (2010-2012) Calder, P, 1998, ‘Dietary fatty Acids and the Immune system’, Nutrition Reviews, Vol. 56, No 1, 70-76 Chauvel V, Vamos E, Paedutz A, Vecsei L, Schoenen J, Multon S, 2012, ‘Effect of Systemic kynurenine on cortical spreading depression and it’s modulation by sex hormones in rat.’ Exp Neurol Aug236(2):207-14 (Relevance to migraine headache) Chih-Chien Sung, Min-Tser Liao, Kuo-Cheng Lu, and Chia-Chao Wu ‘Role of Vitamin D in Insulin’ Resistance Journal of Biomedicine and Biotechnology, Vol 2012 (2012), Article ID 634195, 11 pages doi:10.1155/2012/634195 Dean, W, 2003, ‘Mitochondrial dysfunction, nutrition and aging: the most effective nutrients for defending against age-related mitochondrial decline.’ Townsend Letter for Doctors and Patients, Feb-March 2003 DoctorMyhill.co.uk, ‘Chronic fatigue Syndrome. https://www.drmyhill.co.uk/article.cfm?id=381 viewed 2/09/2009

The

Central

Cause:

Mitochondrial

failure’

Dreosti, I, 1995, Magnesium status and health, Nutrition reviews, Washington: Sept 1995, Vol53, Iss 9, pS23 Ferencik, M, Ebringer, L, 2003, Modulating Effects of Selenium and Zinc on the Immune System, Folia Microbiology, 48(3), p417426 Ford, D, ‘Coenzyme Q10, Muscle Pain and Statins, Are They Related?’ http://EzineArticles.com/?expert=Don_Ford,_M.D viewed 28/01/2013 Gaby, A. 1999, ‘Natural treatment for Osteoarthritis’. Alternative Medicine Review Vol 4 (5): 330-341 Gaby, A. 1999, ‘Alternative Treatments for Rheumatoid Arthritis’. Alternative Medicine Review. Vol 4 (6): 392-402 Lev Gertsik, Russell E. Poland, Catherine Bresee, Mark Hyman Rapaport, ‘Omega-3 Fatty Acid Augmentation of Citalopram Treatment for Patients with Major Depressive Disorder’ J Clin Psychopharmacol. 2012 February; 32(1): 61–64. Last updated Feb-15

doi: 10.1097/JCP.0b013e31823f3b5f Gray, A, 1996. ‘Ginkgo Biloba Extract: A Review’ Altenative Medical Revue, Vol 1(4):236-242) th

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A Practical Guide to Nutrition for Allied Heath Practitioners

Start and Finish Times

Topic or Element DAY 1 Introduction Macronutrients

8:30am – 10:30am

Good Fats / Bad Fats Protein Synthesis and Degradation Practical --- Measuring Body Composition

10:30am – 10:45am

Morning Tea Micronutrients

10:45am – 1:00am

Manifestations of Nutrient Deficiencies Observational Practical --- Micronutrient Deficiencies

1:00pm – 1:45pm

Lunch Inflammatory Mediators

1:45pm – 3:30pm

Insulin Resistance / Type 2 Diabetes Metabolic Syndrome

3:30pm – 3:45pm

Afternoon Tea Fructose

3:45pm – 5:30pm

Appetite Control Gut Health & Food Intolerances

DAY 2 Recap Day One 9:00am – 10:30am

Macronutrient Group Session Chronic Fatigue Syndrome / Fibromyalgia Case Study

10:30am-10:45am

Morning Tea Cholesterol Leptin Resistance

10:45am – 1:00pm

Stress Body Biorhythms Practical --- Abdominal Diagnosis (30mins)

1:00pm – 1:45pm

Lunch Oxidative Stress Antioxidants and Ageing

1:45pm – 3:30pm

Fatty Liver Nutritional Pain Relief Acid / Alkaline Balance Case Study

3:30pm – 3:45pm

Afternoon Tea Osteoporosis Fracture Healing

3:45pm – 5:00pm

Arthritis Discussion on Diets Group Examination END OF SEMINAR

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