Metagenics Update Issue 2

UPDAT E I S S U E 2 • 2019

Do we need to defeat genes to beat obesity?

Modern life: gut feeling something is wrong?

Procrastination busting Turmeric the golden child

Hypothyroidism: underdiagnosed or over treated?

Gut program resolves chronic complaint

• EXCITING NEW PRODUCTS AND RESOURCES • A4M CONFERENCE AUSTRALIA! •

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Contents Every issue

On the cover

9 In the news

4 Hypothyroidism:

Metagenics Personalized Lifestyle Medicine Centre embodies the future of healthcare

10 FAQs Frequently asked questions of our Clinical Support Team

16 Clinical resources

Sara Gottfried - BRAIN BODY DIET: 40 Days to a Lean, Calm, Energised and Happy Self

11 New Clinical Tools

Exciting new tools and product announcements

underdiagnosed or over treated?

Have you considered if it could be other drivers contributing to your patient’s illness, and not solely suboptimal thyroid function?

8 Gut program resolves chronic complaint

14 Modern life: gut feeling something is wrong?

How common modern lifestyle practices may contribute to compromising the health of our gut microbiota.

18 Do we need to defeat

genes to beat obesity?

Why obesity may not be an individual’s fault, but it is their responsibility.

9 Turmeric - the golden child 12 Procrastination busting Don’t procrastinate! Dedicate 7 minutes to read how to bust your procrastination habit and get stuff done!

Find us on Social Media

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Coming to Australia for the First Time...

Targeting Stealth Drivers for Optimal Outcomes A4M and Metagenics have partnered to host a not to be missed event, exploring the drivers of fatigue. Featuring world-renowned Functional Medicine expert, Dr Andrew Heyman, along with one of Australia’s leading Naturopaths, Amina Eastham-Hillier, this two-day event will showcase the latest cutting-edge research and interventions in patients with chronic fatigue. Gain clinical insight from industry leaders on the latest evidence that fatigue may not be a simple energy deficiency, but driven by underlying pathology, such as thyroid and HPA axis dysfunction, mast cell activation, stealth infection and biotoxin illness. Leave the event armed with knowledge and tools to create life-changing results, for your patients presenting with fatigue.

21st - 22nd September 2019 Pullman on the Park, 192 Wellington Street, Melbourne in partnership with a4m

Speaker Panel

YOUR INVESTMENT: Standard: $595 incl. GST MD, MHSA

*Attendees of The International Congress on Natural Medicine are eligible for earlybird pricing ($495 inc. GST) to 21st June 2019.

TO BOOK: BHSc (Nat)

BHSc (Nat)

Call Customer Service to reserve your place!

1800 777 648 (AUS), 0508 227 744 (NZ) or +61 7 3117 3300 (International).

Register your interest at metagenics.com.au/A4M or for more information visit A4Mconference.com.au

Full speaker bios and program agenda available from a4mconference.com.au

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SEMINAR REVIEW

Hypothyroidism: underdiagnosed or over treated?

Have you considered if it could be other drivers contributing to your patient’s illness, and not solely suboptimal thyroid function?

Written by NATHAN ROSE Clinical Education Manager

N

atural Medicine Practitioners have a healthy respect for the importance of thyroid function and are known to go above and beyond the conventional approach to thyroid screening. In truth, the thyroid gland is vulnerable to various contemporary stressors, such as circadian rhythm disruption,1,2 unprecedented exposure to endocrine disrupting chemicals (EDCs),3 chronic stress4 and dysbiosis.5 However, there is question over whether it is necessary to perform in-depth testing of thyroid function to uncover subclinical hypothyroidism that may have slipped through the cracks of conventional screening. Likewise, there is debate over whether correcting thyroid biomarkers to a narrow putative optimal range has benefits over sitting in the conventional range. Finally, symptoms linked to hypothyroidism are nonspecific and frequently experienced by many patients. Thus, it is worth considering whether the contribution of suboptimal thyroid function in a patient’s presentation could be overstated, and if other drivers could be responsible for their illness.

These conundrums highlight the challenges in discerning the role of thyroid function in patients’ health and the following is an attempt to help wade through the complexities. To explore these contentions, let’s first review testing thyroid parameters.

The TSH debate When it comes to thyroid stimulating hormone (TSH), there is a commonly held belief that as a standalone test, it is not an accurate indicator of thyroid function and the conventional ranges are too broad. There is concern that TSH by itself is crude and will not detect a large proportion of subclinical hypothyroidism cases, leading many patients to ‘fall through the cracks’ and continue to suffer from suboptimal thyroid function.

However, a review of recent research reveals TSH reflects thyroid hormone concentration and activity. In fact, TSH has demonstrated that it beautifully reflects circulating thyroid

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hormone levels with a log-linear relationship.

What this means is, if circulating thyroid hormone levels alter slightly, there will be a marked change in TSH levels – thus TSH reflects subtle changes in thyroid function.

For this reason, expert organisations concur that TSH is the most reliable indicator of thyroid status at the tissue level.6,7

Do the TSH goal posts need to change?

If TSH is accepted as a valuable marker, there is still the contention around current ranges being too broad. Some researchers and clinicians have challenged the conventional TSH range and suggested the TSH upper limit should be reduced to 2.5 mIU/L.8 From this perspective, a TSH above this level would be considered subclinical hypothyroidism, and efforts should be employed to lower the patient’s TSH levels, ideally to around 1.0 mIU/L. It seems the data supporting a lower TSH may have been taken out of context in terms of recommending treatment. Studies show that most people with normal thyroid function, especially people under the age of 50, have a TSH below 2.5 mIU/L.9,10 However, TSH levels can fluctuate significantly with time of testing (TSH is higher in the morning), sleep deprivation, strenuous exercise, or working during the night or evening shifts.11 These factors may account for the findings that healthy people can record fluctuations of up to 1.6 mIU/L over a year of monthly testing, i.e. they can regularly fall in the 2.5 – 4.5 mIU/L zone.12 Essentially, the TSH range of 2.5 – 4.5 mIU/L can be seen as a ‘buffer zone’ that allows for normal variation.

“While there may be some controversy about where the normal range for TSH should lie, current clinical guidelines are clear that a TSH in the upper normal range does not reflect hypothyroidism” - Sheehan MT et al13 Another way of exploring this topic is to examine the outcomes of hypothyroidism

treatment, whereby the patients’ TSH levels returned to the conventional TSH range. For instance, in a controlled-trial, administering escalating doses of thyroxine therapy to hypothyroid patients found no differences in measures of wellbeing or quality of life in those who achieved a TSH target of 0.3, 1.0, or 2.8 mIU/L, respectively.14 These results suggest there is not an ‘optimal’ zone in the normal TSH range.

Based on the current evidence, there is little to no clinical benefit in becoming fixated on trying to reduce TSH to sit in the lower end of the normal range. If a patient’s TSH is within conventional parameters and still has health complaints, then it is unlikely to be attributed to thyroid dysfunction, and it would be prudent to consider other causes of their symptomology.

Does reverse T3 offer clinical utility?

The clinical relevance of reverse T3 (rT3) has also been questioned by researchers. There is a school of thought that hypothyroidism may be due to a diversion of T4 to rT3 instead of T3. In this model, there is an inhibition of the enzyme deiodinase 2 that converts T4 to T3 and an increase in deiodinase 3, which instead converts T4 to rT3. Typically factors such as stress and inflammation are proposed to mediate this enzymatic railroading of T4 to rT3.15 Whilst the intricate biochemistry of thyroid hormone metabolism in peripheral tissues via deiodinase enzymes appears attractive and plausible, when compared to clinical observations, it becomes clear that rT3 is yet to demonstrate clinical utility. Moreover, the data points to any changes in T3 to rT3 ratios as a beneficial homeostatic mechanism rather than a pathological driver of h ypothyroidism.

Reason being, rT3 is a metabolically inactive form of thyroid hormone and researchers believe that T4 is diverted to rT3 to help fine tune metabolism to match the body’s needs.

The increased diversion to rT3 becomes critical during times when metabolism is slowed to benefit the host, such as during severe caloric restriction or heart failure, as a process of energy conservation.16

SEMINAR REVIEW

Outside of these scenarios, which would rarely be seen in a Natural Medicine practice, measuring rT3 probably provides no clinical insight. With respect to hypothyroidism, research shows rT3 to be low, rather than high, as the body in this instance is trying to provide as much active T3 as possible to restore metabolism. Overall, after 40 years of investigation, current research suggests rT3 is not a particularly useful biomarker of thyroid function.17

“Measuring serum reverse T3 levels has not, in general, proven clinically useful for the diagnosis of hypothyroidism…

Few clinical situations require measurement of reverse T3 levels.”

-Gomes-Lima C et al18

Elevated TSH and normal thyroid hormone levels TSH 5-10 mIU/L

Symptoms of hypothyroidism

3-6 month trial of thyroid management with continuation if symptoms benefit

TSH >10 mIU/L

Check TPO antibody

Treatment with levothyroxine recommended. Practitioner to refer to Doctor.

Positive

Negative

Consider thyroid support or annual thyroid function tests, depending on patient preference

Thyroid function tests every 3 years

Figure 1: Subclinical hypothyroidism decision tree. Adapted from Vaidya B et al24

Thyroid testing essentials

Managing subclinical hypothyroidism

While research indicates TSH is the most suitable test for screening thyroid function in patients, there are two other tests to date that may have clinical utility. Firstly, free T4 is beneficial when TSH is elevated to determine subclinical versus overt hypothyroidism. Note however, there is some debate on the reliability conventional immunoassay testing, as such, where finances and availability permit, the use of the gold standard free T4 by equilibrium dialysis is preferred.19 The other test to be considered if TSH is elevated, is anti-thyroid peroxidase (TPO) antibodies. These antibodies are a hallmark of autoimmune thyroid disease, especially Hashimoto’s thyroiditis. That said, elevated anti-TPO antibodies alone are not diagnostic of thyroid disease, as a significant portion of healthy subjects can possess high levels.

Elevated anti-TPO antibodies in conjunction with TSH outside normal range suggests thyroid disease.20

Perhaps the bulk of thyroid complaints seen in clinical practice would be what conventional endocrinology classifies as subclinical hypothyroidism - elevated TSH (>4.5 mIU/L [typically values between 4.5 – 10.0 mIU/L]) and normal free T4. In this instance, the data is mixed on the benefits of thyroid hormone replacement. For example, in subclinical hypothyroidism, administrating thyroxine has not demonstrated improvements in inflammation,21 cognition in the elderly,22 fatigue, mood and weight.23,24 In contrast, there has been improvements seen in infertility,25 high cholesterol,26 CVD risk,27 and cognition problems in children.28 Considering the information thus far, subclinical hypothyroidism can be viewed as a condition that does not warrant excessive alarm or need for rapid, aggressive therapy. Certainly, it would be ideal to see TSH levels return to the normal range, and interestingly, up to 65% of cases of subclinical

hypothyroidism have been found to resolve over time without intervention.29 Albeit, there are instances whereby a targeted approach should be taken to normalise TSH, such as: • Anti-TPO antibodies are elevated; • There is a family history of thyroid or cardiovascular disease; • Cognition issues in children; • TSH >10 mIU/L; • The patient has current cardiovascular disease or associated risk factors (e.g. dyslipidaemia, hypertension), goitre, ovulatory dysfunction, infertility, recurrent miscarriages or clinical symptoms of hypothyroidism.30,31,32 Figure 1 illustrates an algorithm to guide decision-making in cases of subclinical hypothyroidism.

Natural thyroid support There are several ingredients that have been shown to help manage subclinical and overt hypothyroidism, including lowering TSH and increasing free T4. These ingredients, rather than replacing deficient thyroid hormone, act

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SEMINAR REVIEW

Table 1: Recommended dietary intake (RDI) and upper limit of iodine.35

Age

RDI

Upper Limit

1 to 3 years 4 to 8 years 9 to 13 years 14 to 18 years Men Women Pregnancy Lactation

90 µg/day 90 µg/day 120 µg/day 150 µg/day 150 µg/day 150 µg/day 220 µg/day 270 µg/day

200 µg/day 300 µg/day 600 µg/day 900 µg/day 1100 µg/day 1100 µg/day 1,100 µg/day 1,100 µg/day

by mitigating stress that impedes the thyroid and provide the nutrients that help catalyse thyroid hormone synthesis.

Iodine deficiency is a common and concerning issue in Australia and New Zealand, and a condition which clearly impedes thyroid function.34,35 Iodine is a unique mineral, as it is thought that its only biological function is for incorporation into thyroglobulin for thyroid hormone synthesis. This considered, iodine has a small therapeutic window and doses even moderately higher than recommended amounts may actually have suppressive effects on thyroid function, especially in Hashimoto’s thyroiditis.36,37 The current Australian recommended daily intake (RDI) for iodine is 150 µg/day, with the upper level intake for adult men and women 1100 µg/day (Table 1).38 When using iodine therapeutically in patients with thyroid dysfunction, evaluate total combined daily intake of iodine and monitor thyroid hormone levels if altered thyroid function is suspected.39

The minerals zinc and selenium have been studied together and in isolation, with results demonstrating safe and effective thyroid support.41 Additionally, a review of 16 clinical trials on the use of 80-200 µg/day of selenium for the management of Hashimoto’s thyroiditis found it significantly lowered anti-TPO antibodies after three months.42 Finally, in a placebo-controlled trial, the adaptogen Withania somnifera was shown to improve thyroid parameters in patients with subclinical hypothyroidism. After eight weeks of treatment, patients receiving withania recorded a significant reduction in TSH and elevations in fT3 and fT4, whereas these parameters were unchanged in the placebo group.43

Drivers and masquerades of hypothyroidism If a patient is found to have subclinical or overt hypothyroidism, then the Functional Medicine approach is to acknowledge that some endogenous and/or exogenous stressor may

be behind the pathology. Circadian rhythm disruption,44,45 psychological stress,46 EDCs,47 mould biotoxins48 and dysbiosis (particularly small intestinal bacterial overgrowth [SIBO])49 have all been found to place strain on the thyroid, such as elevate TSH and in some cases lower T4. Ergo, in addition to providing herbal and nutritional support for the thyroid, equal attention should be placed on identifying and eradicating the thyroid stressor.

If a patient presents with symptoms of hypothyroidism yet TSH is in range, even the higher end of the normal range, it is very likely that the patient has normal thyroid function and there are other causes of their symptoms. In this scenario, a deeper dive into thyroid biomarkers will not identify a hidden hypothyroidism, and it would be more productive to screen other areas that may masquerade hypothyroidism.

Nutrient deficiencies, dysbiosis,50 mast cell activation syndrome (MCAS)51 and chronic infection52,53 may all produce symptoms akin to hypothyroidism, warranting a thorough screening to identify the real culprits.

In summary, the current data suggests the standard tools of assessment and conventional ranges are adequate for screening hypothyroidism. Subclinical hypothyroidism typically isn’t a significant red flag, therefore a slow and conservative approach to management may be preferable.

Furthermore, it would be valuable to be cognisant of other causes or drivers if the patient presents symptomatic, but is biochemically euthyroid by standard measures.

Resolving Chronic Inflammation: Flicking the Switch, From Disease to Resolution Join us at the Metagenics seminar to learn about new frameworks and exciting tools that address novel and complex drivers of chronic unresolved inflammation.

EXTENDED LEARNING SESSION WITH:

YOUR INVESTMENT:

DR SARA GOTTFRIED MD

Sydney | Melbourne

LARA BRIDEN ND

Brisbane | Adelaide

DR ADRIAN LOPRESTI

BA (Hons), MA, PhD Perth

Seminar Session with Metagenics Speakers Account holders: $55.00 incl. GST Students: $35.00 incl. GST Non-account holders: $110.00 incl. GST

Extended Learning Session with Guest Speaker Additional $55.00 inc. GST.

The Metagenics speakers will be presenting at 44 different venues throughout Australia!

Exclusive to selected capital cities only, you can further your learning experience by attending the optional Extended Learning Session.

These sessions are held prior to the Metagenics seminar presentations and are presented by esteemed thought leaders from the Natural Medicine industry.

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Call Customer Service now on 1800 777 648 to reserve your place today!

C ASE STUDY

Gut program resolves chronic complaint

The patient in question is an 88 year old female, who has always been health conscious, and consumed what the Practitioner has described as a “reasonably good diet.” Despite this, she has suffered from chronic loose bowels for the majority of the last two decades; which began when she contracted a parasite while travelling overseas in the late 1990s. Things took a turn for the worse in 2012 when she was hospitalised with acute gastroenteritis. While receiving treatment with Flagyl*, the patient recalls this therapy “stripped her bowel” to the point where she believes she actually passed a section of her gut lining. This traumatic experience had a dramatic effect on her health, to the point where she became concerned for her life.

While the patient went on to obtain significant relief whilst at a reputable NSW health retreat, some months after her stay the loose bowels returned. This relapse took an incredibly heavy toll on her emotional health, as the longevity of the condition began affecting her outlook. She developed a notable level of angst and signs of depression.

Around June 2018 all her bowel movements became explosive, to the point where she was simply passing water. It was at this point that she sought Leoni Gardner’s help and after taking a careful case history, she ordered a number of pathology tests including a comprehensive digestive stool analysis (CDSA). Among results, it was revealed there was a low level of beneficial bacteria, *Flagyl, generic name metronidazole, is an antibiotic and antiprotozoal medication used to treat a variety of infections.

Treatment regimen The Practitioner prescribed the Metagenics Gut Pathogen Elimination Program, Figure 1, using Antimicrobial Herbs for the Management of Dysbiosis as the chosen antimicrobial to address the patient’s gastrointestinal symptoms. This program corrects dysbiosis and helps restore healthy gut microbiota diversity and function, while supporting gastrointestinal barrier integrity and elimination pathways (Table 1).

Weeks 1 & 2 (2 Weeks)

Case history

and an opportunistic overgrowth of Candida albicans and Klebsiella spp.

Massive improvements in a short space of time At baseline, the patient’s stools resembled type 7 according to the Bristol Stool Chart (BSC) (Figure 2).

• Weeks 1 & 2: The patient began on the first phase of the regimen and after 7 to 10 days her stools began moving from type 7 to 6 on the BSC. She reported her bowels were more consistent, and not explosive.

• Week 3: At this stage there was a massive improvement, as her stools started to resemble type 4 and 5 on the BSC. She was also feeling less stressed and more hopeful about her health, and her energy began to improve.

• Week 4: The patient maintained 100% compliance throughout the four week period and was now producing well-formed stools three times daily. There was much less flatulence and significantly reduced urgency.

This represented a remarkable turnaround.

The anxiety, depression and her obsessive pre-occupation with her bowel movements all reversed and this gave her an entirely new lease on life!

“I am so grateful for Leoni’s careful study of my condition, and the remedies she thoughtfully prescribed to put the situation right. Everything is perfectly normal these days, probably better than I’ve ever had, even since my teenage years! Thank you Leoni!”

Long lasting relief Six months on, the patient’s bowels continue to function well. At almost 89 years of age she now enjoys a full life with great health. Her outlook is positive and she engages in various recreational and community activities.

Weeks 3 & 4 (2 Weeks)

W

hen a person’s life revolves around their ‌ proximity to bathroom ‌facilities, it can be demoralising and affect their sense of freedom and engagement in day-to-day activities.

This case tells of an elderly patient who suffered from debilitating loose bowels for the better part of 20 years, until Leoni Gardner, Practitioner from Kempsey NSW, turned her life around with the Metagenics Gut Pathogen Elimination Program.

Gut Pathogen Elimination Program

Rationale

Antimicrobial Herbs for the Management of Dysbiosis

To manage dysbiosis and maintain healthy gut microbial balance.

Glutamine & Boswellia (BosPure® Boswellia) for Intestinal Integrity

To soothe, protect and promote gastrointestinal integrity.

Strain Specific Probiotics for Gut Microbiota Restoration and Support

To promote digestive secretions to aid digestion, optimise assimilation of nutrients and support detoxification. To maintain optimal acidity and terrain for microbial balance.

Dandelion, Ginger and Meadowsweet for Healthy Digestion

To rebuild native commensal bacteria, suppress pathogenic organisms, and support barrier integrity and function.

To reduce toxic load by supporting gut barrier function, Milk Thistle, Green Tea microbiome health and and Amino Acids for lipopolysaccharide (LPS) Optimal Detox reactions, improve cellular liver detoxification capacity, as well as conjugate and eliminate toxins.

Detox Greens

To protect the integrity of the gastrointestinal mucosa, improve detoxification capacity and support healthy gut bacterial balance.

Strain Specific Probiotics for Gut Microbiota Restoration and Support

See Detox Foundations

Dandelion, Ginger and Meadowsweet for Healthy Digestion

See Detox Foundations

Figure 1: Metagenics Gut Pathogen Elimination Program.

BRISTOL STOOL CHART Type 1

Seperate hard lumps, like nuts (hard to pass)

Type 2 Sausage-shaped but lumpy Type 3

Like a sausage but with cracks on it’s surface

Type 4

Like a sausage or snake, smooth and soft

Type 5

Soft blobs with clear-cut edges (passed easily)

Type 6

Fluffy pieces with ragged edges, a mushy stool

Type 7

Watery, no solid pieces, entirely liquid

Figure 2: Bristol Stool Chart (BSC).

Thanks to Leoni Gardner of Kempsey NSW, for providing this case study.

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Turmeric the golden child

T

he cultural and medicinal history that surrounds Curcuma longa, commonly known as turmeric, and its associated constituents has encouraged decades of research into its biological and pharmacological benefits.1 Extensive clinical trials over the past century have shown that curcumin, a constituent of this golden spice, can modulate inflammation and influence multiple cell signalling pathways, as well as exert antioxidant, antimicrobial, antiviral, antifungal, analgesic and antiplatelet properties.2 Interestingly, curcumin-free turmeric formulations have demonstrated therapeutic capacity, which indicates there is more to turmeric than curcumin alone.3

BCM-95™ Turmeric, more than the sum of its parts BCM-95™ Turmeric stands apart from other forms of turmeric because it is a whole turmeric extract, which does not contain any non-turmeric components, unlike many other formulations.4 Standardised to contain therapeutic doses of curcuminoids, this unique composition comprises a synergistic blend

Combination

BCM-95TM BosPure® Turmeric Boswellia

of the most active and potent components of turmeric, curcuminoids and aromatic compounds. BCM-95™ has proven synergistic activity working to increase free-curcumin bioavailability, providing multifaceted health benefits. BCM-95™ is a highly bioavailable, therapeutically active all-in-one natural formulation which includes all of the active and potent components of turmeric, working to support health outcomes.5

The bioavailability conundrum It is well understood that a major barrier to turmeric’s clinical efficacy is its poor bioavailability. To overcome this problem many other formulations have included the use of adjuvants such as piperine, liposomal curcumin, curcumin nanoparticles and curcumin phospholipid complexes. Such efforts have unfortunately not contributed to identifiable clinical or biological results.6 The whole turmeric extract of BCM-95™ as a therapeutic agent does not solely rely on its bioavailability, but rather its medicinal benefits arising from its positive influence on gastrointestinal health.

BCM-95™ has been found to influence the

Additional ingredients

diversity of gut microbiota, reduce intestinal permeability, inflammation, oxidative stress and support barrier function, all of which have wide ranging influences on both intestinal and systemic health.7

Clinically effective turmeric In addition to its enhanced bioavailability, BCM-95™ Turmeric is a clinically trailed extract with demonstrated safety. Positive outcomes have been observed for various conditions, including inflammatory disorders such as osteoarthritis8 and rheumatoid arthritis (RA).9 This well-researched extract also has a place for depression, as two randomised clinical trials have shown that 25 g/day of BCM-95™ provides significant benefits to patients with major depressive disorder.10,11

Revival of an ancient remedy Boswellia serrata gum resin is an ancient herb traditionally used as an analgesic, anti-rheumatic, antispasmodic, anti-arthritic, and anti-inflammatory.12 The potent antiinflammatory properties of boswellia are owed to the biological activity of boswellic acids,

When to use

High Potency Antiinflammatory Herbs.

Salix alba, Zingiber officinale, Quercetin, Citrus bioflavonoids, Capsicum frutescens.

• For temporary relief of pain and inflammation.

• For relief in acute and painful conditions.

BCM-95™ Turmeric & Devil’s Claw to Treat Chronic Inflammation.

Harpagophytum procumbens, Piscidia piscipula.

• Relieve arthritis pain due to mild inflammation.

• Assist with nerve, joint and muscle pain.

• Decrease inflammatory response within the body.

• For relief in chronic painful conditions.

BCM-95™ and Saffron for Depression.

Crocus sativus.

• Support healthy mood balance including major depression, modulate neurotransmitters.

Glutamine and Boswellia (BosPure® Boswellia) for Intestinal Integrity.

Larch arabinogalactan, Zinc bisglycinate, Vitamin A, Vitamin D3, Aloe vera.

• Relieve gastrointestinal discomfort, pain and inflammation.

• Protect gastrointestinal mucosa and gut integrity.

Detox Greens

Gallium aparine, Arthrospira platensis, Glycyrrhiza glabra, Aloe vera, Coriandrum sativum, Fucus vesiculosus, Glutamine, Potassium, Larix arabinogalactan, Pectin,Zinc.

• Supports gastrointestinal and kidney detoxification.

• Support alkalinity to assist with waste excretion.

• Supports functional and healthy gut bacterial balance.

Figure 1: BCM-95TM turmeric was shown to be significantly more bioavailable than standard turmeric extract in human participants.7

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IN THE NEWS

Research

Bites been purified to contain minimal levels (<5%) of pro-inflammatory β-boswellic acid (BBA).14 This is noteworthy, as some commercial boswellia extracts can contain as little as 2% AKBA, and as much as 25% BBA.15 BosPure® has been created to enhance systemic absorption of the favourable boswellic acid AKBA for better therapeutic outcomes.

Together is even better

of which 3-O-acetyl-11-keto beta-boswellic acid (AKBA) is historically regarded as the most active and therapeutically valued component.13

More bang from your ‘bos’ BosPure® is a proprietary boswellia extract from wild crafted gum resin, containing no less than 70% boswellic acids. BosPure® has

Research supports the combination of turmeric and boswellia for greater efficacy in a variety of inflammatory conditions due to their synergistic activity .16 In a 2018 study, over 200 patients with severe osteoarthritis (OA) found that curcumin in combination with boswellia was more effective at reducing pain related symptoms.17 This study highlighted that the combination of curcumin and boswellic acid work collaboratively to increase treatment outcomes, providing you with the confidence in supporting therapeutic outcomes in your patients.

Commuting via nature enhances mental health. Findings published by a European research collective reveal that commuting through natural environments brings better mental health, regardless of whether travelling on foot or by bike, car or public transport.1 Data on commuting behaviour from 3,599 adults across four cities was analysed based on travel exposure to trees, parks, forests, and natural water landscapes; how often the participants traversed through such environments, mode of transport, and quality of mental wellbeing using a validated scale.

Researchers found that the greatest benefits in mental health came with active transport (e.g. cycling, walking) with even greater benefit for those commuting through natural environments compared to those whose did not. Re-routing how a patient arrives or leaves the workplace calling on the healing power of nature to mentally meet the needs of modern life.

In the news Metagenics clinic embodies the future of healthcare Leading the frontier in how medicine is practised in the 21st century, the Personalized Lifestyle Medicine Centre (PLMC) recently opened in Gig Harbour, Washington. A shared vision of Jeffrey Bland, PhD; Brent Eck, Metagenics Inc. CEO; and Joseph Lamb, MD; the PLMC will comprise a clinical research laboratory as well as a state-of-the-art medical clinic for patients.

“I’m so pleased to see the opening of the Gig Harbor Personalized Lifestyle Medicine Centre that – through its excellence in patient management and research efforts – will accelerate the availability and adoption of this important approach to the prevention and management of chronic disease.”

- Dr Jeffrey Bland Providing healthcare to members of the public, the PLMC combines Metagenics’ experience in Functional Medicine research with the best practice in Clinical Medicine – with

the fundamental goal of matching this personalised approach to health to each individual’s needs. Based on the concepts of Functional Medicine which view the body as an integrated system, therapeutic programs are tailored to each patient using nutritional and herbal interventions to address the multitude of factors driving chronic disease, Dr Michael Stone, Brent Eck, Dr Jeffrey Bland and Dr Joseph Lamb together with dietary and at the launch of the Personalized lifestyle recommendations Lifestyle Medicine Centre. to improve health status and quality of life.

With the support of Metagenics, a significant element of the being gathered in order to make correlations PLMC will be its ground-breaking research among genes, the microbiome, diet, blood program, LIFE-HOUSE (Lifestyle Intervention markers, and similar factors, with the goal of and Functional Evaluation – a Health OUtcomes helping to make predictions for therapeutic SurvEy), proving that the personalised lifestyle programs. The vision for this project is that medicine model works. Team members, Joseph excellence in care will benefit the individual, Lamb, MD; Michael Stone, MD; Deanna Minich, with widening ripples of influence on their PhD; and Metagenics Institute Chief Medical workplaces, families, and communities. With a Officer, Sara Gottfried, MD have built a truly view to making personalised medicine the new unique clinical-trial model which gathers standard of care, the PLMC is helping to change specific data on patients. Information is the face of healthcare into the future.

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FA Q

FAQ Frequently asked questions of our Clinical Support Team.

Q: How do you know if probiotic strains work together and play nicely in a multi-strain probiotic formulation?

Q: How does Lycium Hypothyroid Support compare to Mood, Adrenal and Thyroid Support for low thyroid function?

A: In the last two to three years there has finally been scientific papers published investigating multi-strain probiotic combinations.11,12 The early evidence is revealing probiotic strains do not compete in the capsule or gut, and that overall, antagonistic effects are unlikely. That said, this is best confirmed by extensive quality testing.

Metagenics can confirm the strain combinations found in our multi-strain probiotics do not negatively interact thanks to a rigorous testing regimen that is well beyond the industry-mandated testing for probiotics. This process includes quantifying all strains independently before blending, retesting immediately after encapsulation, and retaining samples of every batch to continue to test at various intervals up until (and even past) expiry.

Within High Strength, Researched Probiotic Strains, there are five strains, made up of four different species, and one yeast. They are: Lactobacillus acidophilus (NCFM®), Bifidobacterium lactis (Bi-07), Lactobacillus rhamnosus (HN001™), Bifidobacterium animalis ssp lactis (HN019™) and Saccharomyes cerevisiae (boulardii). The current testing technology available can detect down to the species level. Thus, while this technology can not differentiate between two Bifidobacterium strains, the Bifidobacterium strains can be quantified individually before encapsulation and the total input can be confirmed right up until expiry, confirming the individual strains have not been impacted. This can however, become increasingly complicated when there are more than two of the same species within one formula.

Metagenics’ commitment to using clinically trialed probiotic strains and strengths, which are subject to rigorous quality processes, ensures probiotic combinations cooperate from encapsulation to expiry for the best therapeutic outcomes.

A: Lycium Hypothyroid Support is recommended in cases of primary hypothyroidism, as it contains a combination of herbs and nutritional cofactors, such as iodine, selenium, zinc and vitamin E to support the synthesis and regulation of thyroid hormones.1 Traditionally used for fatigue, Lycium barbarum also features as a potent antioxidant,2 alongside Withania somnifera which has been demonstrated to boost thyroxine (T4) levels.3 Rosmarinus officinalis adds value as an antioxidant and circulatory stimulant, as does warming Zingiber officinale.4 Based on these mechanisms, this combination is well placed for sluggish thyroid activity and associated symptoms, such as lethargy, low metabolism and poor circulation.

On the other hand, Mood, Adrenal and Thyroid Support is relevant in cases of hypothyroidism driven by stress. Increased activation of the hypothalamic-pituitary-adrenal (HPA) axis can directly impair normal thyroid function, and stress-induced changes in neuroplasticity and reduced cellular metabolism may also contribute to low mood.5 The key ingredients within Mood, Adrenal and Thyroid Support, such as withania and Rhodiola rosea work to modulate HPA activity, improve stress resilience and decrease the oxidative effects of excess glucocorticoid exposure.6 Moreover, Hypericum perforatum,7 rhodiola,8 SAMe9 and folinic acid10 promote an adaptive neurological response by increasing neurotransmitter activity and providing mood support. This considered, this combination is suited for patients with low thyroid function who are stressed, and presenting with low mood and/or anxiety.

In essence, both combinations support healthy thyroid function, however their application may be guided by the underlying driver and presentation of hypothyroidism.

CHANGING THE FUTURE OF HEALTH with SYSTEMS THINKING Last month, One Health trained 6 bi-cultural workers from communities with high refugee populations in Systems Mapping and this month, they are using it to help us better understand the complex barriers to health and wellbeing in their own communities.

Following that, we’ll fund the solutions!

To change the system, you first need to map it

Follow our work at 10

onehealthorganisation.org

NE W CLINIC AL TOOLS

PRODUCT ANNOUNCEMENTS

New clinical tools MetaBiome™ Microbiome Sampling Kit A Comprehensive Test for Microbiome Composition and Function.

Simple, non-invasive sampling performed at home and conveniently posted in the supplied reply paid envelope for assessment.

Contents: Each kit contains: 1 x activation card, sample collection tube, sampling instructions, Bristol stool chart, reply paid sleeve and envelope.

Order code: MBKIT Storage: Store below 30°C MetaBiome™ Microbiome Sampling Kit Process Practitioner

Patient

Microba

Purchase kit from Metagenics $80 (inc. GST) Sell/prescribe kit to patient Activate kit at metabiome.com.au and assign to patient $269 (inc. GST) Total kit cost $349 (inc GST)

Email questionnaires to patient Perform sample and complete questionnaires (optional) Send sample to Microba Assess sample

Receive report and discuss with patient

Omega-3 Index Test Kit An Exciting Tool to Validate and Tailor Your Omega-3 Prescriptions!

A simple, easy to use, validated test that measures red blood cell (RBC) omega-3 essential fatty acid (EPA and DHA) status to personalise supplemental and diet prescriptions.

Contents: Each kit contains 1 x sample collection card, lancet, bandage, gauze pad, alcohol wipe, return envelope Order Code: OQTK Wholesale: $45.00 exc. GST Storage: Store between 15°C to 30°C

Using the test is easy!

1. Register the test kit Go to omegaquant.com/start and complete the easy to use online form.

2. Collect the sample Allocate five minutes during your patient’s consultation and follow the step-by-step instructions to collect their sample.

3. Mail the sample Insert the patient’s sample and collection card in the pre-paid return envelope and drop it in the mail.

4. Get results Within 1 to 2 weeks, you will receive the personalised results via email.

For more information for the above testing kits, contact our Clinical Support Team on 1800 777 648 or reach out to your Area Sales Manager.

Product announcements Proxan (30 and 60 Capsules)

Five Mushroom

Proxan has been upgraded, replacing the cyanocobalamin with mecobalamin.

Proxan is usually prescribed alongside other folate-containing supplements, therefore the folate has been removed to mitigate the risk of exceeding safe prescribing of daily folate in patients taking multiple supplements.

Due to new DNA testing technology, two of the mushrooms in Five Mushroom are now represented differently on the label. The formulation however has not changed and can therefore be trusted to deliver the same therapeutic efficacy. No change to size, order code or price.

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BEST PRAC TICE

Procrastination busting Don’t procrastinate! Dedicate 7 minutes to read how to bust your procrastination habit and get stuff done!

Written by ANGELA CARROLL Programs Manager

With mid-year upon us, it may be time to revisit your to-do list for this year. How is your inbox clean out going? The article you want to write?

Your next blog post? The networking events you intended to attend? The promotional program you desperately need to design? Your marketing plan for the year? Oh wait! Sorry, that is my list!

In all seriousness, what’s on your to-do list that you just haven’t done?

Surprisingly, but not unexpectedly, there is a science to procrastination based in the way you process the organisation of tasks on hand. Understanding this, and then applying some high level coaching skills will help you get those tasks done and achieve more in the remaining months of this year.

12

The science of procrastination When you have made the decision to act, procrastination is not about decision making – it is more about when to act. The decision to get on with the task requires unison between the pre-frontal cortex and limbic system.

As you may be aware, the pre-frontal cortex is involved in the executive functions of: • Emotional control • Task initiation • Activity shifting • Impulsiveness • Self-monitoring • Working memory • General orderliness • Task monitoring • Planning and organisation Consider how many of these functions are required to act ‘in the present’ to get stuff done. Then, consider the influence of the limbic system, which deals with immediate, concrete rewards. It is directly connected to basic emotions which arise in the amygdala.

When you are tired and overwhelmed, or the task is complex or unfamiliar, the limbic system overrides the pre-frontal cortex and you will go for the ‘quick fix’ that is familiar, easy and accessible. Ergo, you procrastinate. For

example, “I’ll just check Facebook, I may need to respond to someone’s comment.” “I’ll put a load of washing on.” “Gosh, those floors/the weeding/the groceries need to be done!”

Procrastination has a scientific equation Professor Piers Steel developed ‘the procrastination equation,’ which suggests decision making can be explained by the following equation:1 Motivation = Expectancy x Value

Impulsiveness x Delay

Motivation indicates how invested, or driven you are to take the course of action. On the top half of the equation are Expectancy and Value. Expectancy refers to how much you expect to succeed at the task and receive a reward (i.e. how achievable you think it is), and Value refers to how much you enjoy doing a task, and how much you’ll enjoy the reward from completing it. On the bottom half of the equation are the variables, Impulsiveness and Delay. Impulsiveness refers to your tendency to get distracted – the more impulsive you

BEST PRAC TICE

Research

Bites are, the less you like to delay pleasure. The last variable refers to your sensitivity to delay, that is, the further away the completion of the task and the reward, the less motivated you will feel.

The theory suggests that you are more likely to take action when the tasks are enjoyable and easy to attain, and you are more likely to procrastinate when the task is unpleasant or the reward of completion is a long way off.

This model can be a useful tool to gauge your ability to procrastinate and help break the habit. Additionally, when you apply it to all the tasks you are delaying, it will help you identify where you may be facing a roadblock.

Once you identify these factors you can apply the process in the following section to successfully bust your procrastination.

Let’s look at an example. You want to create a stand-alone weight loss program in your practice utilising the Shake It Program as an offering for your current patients and to attract new patients.

As part of this exercise, score each variable out of 10. These are self-rated scores to be used to assess the components that are contributing to the procrastination behaviour. In order to move forward and overcome the procrastination you want your scores above the line (Expectancy and Value) to be high and the scores below the line (Impulsiveness and Delay) to be low.

• Expectancy = 9/10 You know you can do it, and it will be great for your clinic.

• Value = 10/10 You know this is a much needed, successful program that will change people’s lives for the better, and is also a highly marketable offering.

• Impulsiveness = 6/10 Every time you sit down to work out the details, you get distracted with other tasks.

• Delay = 5/10 There’s no hard and fast deadline.

In this example, since Expectancy and Value are rated highly, Motivation can be improved by actively managing Impulsiveness and Delay.

Great! So how do you do this?

Following these steps can help resolve your procrastination predicament: • Step 1. Call yourself out on your procrastination. Really own it and the task.

• Step 2. Clearly identify which parts of the equation are the problem.

• Step 3. Do something to fix the problem (See Diving into Step 3).

• Step 4. Break the task down into chunks that you can achieve and work through each chunk in a scheduled manner.

• Step 5. Celebrate your win! Savour the emotion of completing the task.

• Step 6. Move onto the next task through the same process.

Diving into step 3 Fixing the problem (Step 3) will require a little self-coaching. The pre-frontal cortex is a very rational, logical aspect of the brain. In order to take action you need to link this to the amygdala through emotional attachment.

It is the emotions that will move you forward.

Here is the process: 1. Take a quiet moment, and focus on the task you have been procrastinating on.

Think of a current example for yourself as we go through this. Perhaps something you know will make a big impact, but that you are consistently avoiding.

2. Imagine you have completed the task.

What is the positive impact on your life/ business? Is this impact bigger than the other tasks you’ve been consistently prioritising over this task? Visualise the task finished, in all its glory! How does it look?

3. How does this make you feel? It’s finally off your to-do list! Really feel the emotions.

When you are in this emotional state how do you stand? How do you breathe? How do you hold yourself? Emulate this.

4. Now that you have finished and are successful, what words do you say to yourself? Say those words out loud.

5. Keep the completed task in your mind.

What does this mean for you now that you have been successful? How will your life improve? Will it improve the lives of others?

6. Celebrate this feeling!

7. Harness how you feel right now. What steps can you start immediately to get this task underway? What do you need to complete the task? Write these down. When can you do them? What has to change in order to get these steps underway and the task completed?

8. Write down how you will hold yourself accountable and relevant due dates.

9. Take action. Now!

Procrastination busting in action I am going to practice this method moving forward, and I encourage you to try it.

Make the remainder of the year proactive and productive. Wishing every success for you now and always. I would love to hear how you apply this and about your achievements. Send me an email at acarroll@metagenics.com.au

Metabolic syndrome a red flag for low vitamin C. Metabolic syndrome (MetSyn) has been linked to vitamin C deficit according to recent research.1 Literature shows that dysbiosis, inflammation, and release of endotoxins in MetSyn collectively impair vitamin C uptake within the gut.

Specifically, dysbiotic endotoxin, lipopolysaccharide (LPS) blocks the uptake of ascorbate and its oxidised form (dihydroascorbate), promoting a cycle of inflammation and barrier dysfunction.

Researchers highlighted that vitamin C repletion could potentially moderate disease severity by restoring barrier integrity and bolstering antioxidant defenses.

Covering the bases of functional wellbeing, a simple script of vitamin C might be the key to unravelling the gridlock of MetSyn! Plantarum 299v counters resistant superbug. Probiotics chalk up another win for immunocompromised patients at risk of contracting antibiotic-resistant bug, Clostridium difficile (CD).2 Findings from 5,341 patients receiving organ transplants revealed that a prophylactic daily dose of 10 billion CFU (organisms) of Lactobacillus plantarum 299v reduced the annual rate of CD infection from 18 cases down to 2 (p= 0.0003). Further, life threatening consequences of CD infection were much lower in the year following the trial, indicating probiotic success in preventing the serious infection. Providing protective assurance, Lactobacillus plantarum 299v raises the standard of care for patients at risk of Clostridium difficile.

Antioxidants cut NSAID use in endometriosis. Antioxidant allies have been shown to reduce severe pain in endometriosis and lower the use of pain medication.5 Nearly 400 endometriosis patients received a combination of N-acetyl cysteine (600 mg), alpha lipoic acid (200 mg), bromelain (25 mg) and zinc (10 mg) for 6 months. Results indicated that the number of participants experiencing severe pain (rated >8/10) fell from 40% to 3.6%, with over half classifying their pain as relatively mild (<3/10) (p< 0.0001) following antioxidant treatment.

Further, the number of patients taking NSAID medications reduced from 86% to 37%. Offering innovative treatment options for chronic pelvic pain, Natural Medicine supports women with endometriosis.

13

KEY CLINICAL CONCEPTS

Modern life: gut feeling something is wrong?

How common modern lifestyle practices may contribute to compromising the health of our gut microbiota.

Written by LAURENCE KATSARAS Clinical Resources Manager

In the civilised world the microbiome is now subject to a constant onslaught of factors which are detrimental to its diversity, and as such, it bears the brunt of modern stressors. While industrialisation has seen great improvements in public health and longevity, the increase in antibiotic use, caesarean section births, formula-fed infants, heightened medication prescriptions, coupled with a lack of exercise and dramatic dietary changes has had vast implications on microbial health. Although modern civilisation has granted us many advantages, the gut microbiota has been pushed into an altered state of health, leaving the host susceptible to chronic disease. Long-term health of the individual, and perhaps humanity, relies on correcting the health of gut microbiota and offsetting the modern lifestyle practices that compromise it.

The consequences of the modern age The late 19th century is said to mark the time the gut microbiota began to change in developed nations, hallmarked by shifts in the presence of indicator organisms such as H. pylori, and the ratio between Prevotella and Bacteroides species.1 Changes to both microbiota composition and function can have a significant impact on an individual’s health due to the intimate relationship between the host and their microbiota.

Modern research is revealing that the host and microbiota are not autonomous entities, but rather are considered holobionts; whereby

Symbiosis

Immune tolerance

The journey back to symbiosis A concerted approach is required to rehabilitate the altered gut microbiota, including a plant based diet, diversity enhancing lifestyle practices, and clinically proven strain-specific probiotics to support and nourish the existing commensal bacteria. Additionally, addressing inflammation and supporting overall health will also assist in restoring the microbial balance.5 Likewise, minimising exposure to detrimental influences on the gut microbiota must also be considered, such as avoiding overuse of antibiotics (where possible) and reducing intake of refined, processed foods.

Feeding the gut The diversity and function of the gut microbiota can be supported by a diet rich in prebiotics, including fibre and polyphenols, as well as avoiding the standard Western high fat, low fibre foods. Dietary fibre, functionally known as microbiota accessible carbohydrates

Reduction of microbiota diversity

Rich / diverse microbiota

Mucosal barrier

the fitness of one cannot be separated from the other.2 With this symbiotic view in mind, we now understand many critical feedback loops exist between the gastrointestinal microbes and the host to maintain a stable state of homeostasis.3 However, when the system is pushed beyond its limits, it is propelled into an ‘alternative stable state’, that is, a pre-disease or disease state. Just as the feedback system maintains the stable system, it may also maintain an alternative stable system (Figure 1), creating a new normal for the individual, leaving them in a perpetually vulnerable state of health. Supporting the transition back to healthy symbiosis is therefore paramount to achieve optimal long-term health.

RedOx Balance

Increase of permeability

Critical Transition

Low diversity microbiota

Oxidative stress

Increased permeability

Increase of inflammation

Figure 1: Alternative stable states, the shift from symbiosis to altered symbiosis.4

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ALTERED SYMBIOSIS

Sustained low-level inflammation

Oxidative stress

(MACs), represents the main source of energy for gut bacteria. These MACs have the potential to modulate gut microbial composition and function by not only boosting colonisation of beneficial bacteria but also improving short-chain fatty acid (SCFA) production.6 Unfortunately however, the typical Western diet is low in MACs and can result in disruption of gut homeostasis and contribute to the development of various inflammatory and chronic diseases. Conversely, addition of dietary MACs has beneficial effects on the gut microbiota, host metabolism, and immunity.7 A wide variety of specific foods that can increase the production of beneficial fermentation products and improve microbial diversity are included in Table 1. Likewise, dietary habits that can offset the detriments to the microbiota include; avoiding nonnutritive sweeteners, emulsifiers, processed foods, meat manufactured with antibiotics, and dairy products produced with hormones.

Drinking filtered water, using glass, ceramics, or stainless steel instead of plastics when cooking or heating foods to avoid bisphenol A (BPA), bisphenol S (BPS), bisphenol F (BPF), and other harmful chemicals has also been shown to produce benefits to gut microbial health.8

A modern microbiome supportive lifestyle Similar to cultural homogenisation in the modern world, the microbial communities in the gut are suffering from loss of diversity.

While foregoing some of the conveniences of modern life is unreasonable (i.e. sanitation), active steps can be taken to offset some of the associated consequences. Simple interventions such as increasing aerobic activity has been shown to benefit gut microbiota. One recent study put overweight women on an endurance exercise program for six weeks without any dietary changes, and it was found that the exercise alone increased beneficial Akkermansia and decreased pathogenic Proteobacteria.9 Other lifestyle interventions that have been shown to improve microbiota diversity include spending time in nature and having pets.10,11,12 Encouraging patients to implement these simple strategies, along with not being afraid to get their hands dirty – avoiding constant, excessive sanitisation, can have significant impacts on microbiota diversity.

KEY CLINICAL CONCEPTS

Probiotics push it in the right direction Providing patients with dietary and lifestyle advice to restore the gut microbiota should make up the foundations of any treatment plan. However, if individuals are pushed into a detrimental, altered state of symbiosis, more specific interventions known to support the regeneration of their core genera, such as clinically proven probiotic strains, are needed. The most highly researched strains to provide therapeutic restoration to the gut microbiota include: • Lactobacillus rhamnosus (LGG®), which dramatically influences the resident microbiota, promoting the growth and function of five out of the six genera that contain the core bacteria characteristic of a healthy stable state. The net functional benefits include increased butyrate production and altered gene expression of endogenous gut bacteria to increase their flagella, thus enhancing their function.13,14,15,16 • Saccharomyces cerevisiae (boulardii) reduces antibiotic-associated loss of bacteria and rapidly restores the microbiota after use.17 SB has also been shown to increase keystone bacteria that are fundamental to healthy microbiome function.

• Bifidobacterium animalis ssp lactis (BB-12®)

prevents the growth of pathogens and up-regulates the expression of the carbohydrate metabolising enzymes of the commensal bacteria, allowing them to flourish, further supporting the gastrointestinal environment.18,19 These three probiotic strains feature in Strain Specific Probiotics for Gut Microbiota Restoration and Support. Together, they favourably impact the host by improving barrier integrity, modulating the immune system and interacting with the nervous system, ultimately producing multiple core benefits to rebuild diversity and function of the gut microbiota.

Restoration is paramount At this stage in human existence, protection and restoration of gut microbial composition and function is of great importance. As Martin Blaser, Director of the Human Microbiome Program, writes, “restoration of the human microbiome must become a priority for biomedicine.”20 It is therefore imperative to help patients understand the importance of adopting healthy dietary habits and lifestyle practices that support the gut microbiota, alongside the use of clinically proven, strain specific probiotics.

Table 1: A short list of microbiota enhancing foods.

FOS and Inulin Chicory root Garlic Jerusalem artichoke Leek Onion Dandelion green Asparagus

Banana Barley Wheat Sugar beet Honey Tomato Rye

Resistant Starch Potato (cooked then cooled) Banana Cashew nut White beans Lentils

Fibre

Polyphenols

Flaxseed Vegetables Fruit Whole grains

Blueberries Strawberries Peach Plum Cocoa Chocolate

Other Prebiotic Foods Kiwi fruit Beetroot Fennel bulb Green peas Snow peas Sweet corn Savoy cabbage Chickpeas

Red kidney beans Soybeans Cashews Pistachio nuts Peaches Watermelon Grapefruit

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CLINICAL RESOURCES

Clinical resources Sara Gottfried - BRAIN BODY DIET: 40 Days to a Lean, Calm, Energised and Happy Self Smart women are taught to lead with their heads, yet 100 million women suffer from weight gain, foggy thinking, anxiety, depression, addiction, forgetfulness, overwhelm, exhaustion, and other seemingly brain-related problems at double the rate that men experience these symptoms. Leading women’s health expert, threetime New York Times bestselling author, and Chief Medical Officer for Metagenics Institute, Sara Gottfried, M.D. says it’s time to repair the brain/body disconnect.

In her new book, Brain Body Diet: 40 Days to a Lean, Calm, Energised and Happy Self (HarperOne; March 2019), Dr Gottfried’s research demonstrates a vitally important insight about the interconnectedness between the brain and body: you can’t have a healthy brain if your body is out of whack, and you can’t have a healthy body if your brain is out of whack.

The book offers a leading-edge approach to reversing brain/body breakdown and restoring the delicate balance between the two with an evidence-based, easy-to-implement food and lifestyle redesign.

Brain Body Diet reveals how to address the myriad symptoms of an imbalanced brain/body and: • Change the body weight set-point in the brain that makes it so difficult to lose weight.

• Clear out toxins, including dementogens and obesogens that change your mind, generate negative habits and obsessions, make you hungrier and fatigued, and increase your risk of cognitive impairment and memory loss – generally making you not feel like yourself.

• Recover the grey matter lost from pregnancy and/or excess alcohol.

• Regain and stabilise mental health and prevent burnout, depression, and anxiety.

• Deepen sleep, enhance the glymphatic system, and clear more amyloid beta – the potential toxin that contributes to Alzheimer’s disease.

• Reclaim the balance in your gut flora that helps weight loss and prevents inflammation, autoimmunity, and hormone problems.

• Prevent or reverse brain-related neuroinflammation and degenerative

disease, such as memory loss, Alzheimer’s, and multiple sclerosis.

• Create a greater sense of integrated wholeness – what Dr Gottfried calls neurospirituality.

For the first time, Dr Gottfried shares the personal experience that led her to uncover the brain/body axis, how mainstream medicine often fails us, and ultimately how to lose weight and restore health in 40 days by balancing the brain and body to once again work in harmony.

Harvard-educated Physician, speaker, and author of The Hormone Cure, The Hormone Reset Diet and Younger, Dr Sara Gottfried M.D, has produced another sterling piece of work with her new book Brain Body Diet: 40 Days to a Lean, Calm, Energised, and Happy Self.

As a leader in the Functional Medicine movement and practicing Physician, Dr Gottfried’s experience and wisdom is married with the l atest scientific research, and enriched with incredible stories of success.

Her passion for personal lifestyle medicine and addressing the root cause of problems is instilled in this book, calling out limitations of mainstream medicine and illuminating the interconnectedness of the brain and body.

“Certain symptoms reflect a brain body out of balance. These are sacred messages, not diseases to be medicated into submission.”

Brain Body Diet offers readers practical guidance on restoring brain/body harmony, and ultimately reclaiming optimal health and wellbeing.

Brain Body Diet: 40 Days to a Lean, Calm, Energised, and Happy Self is available to purchase through numerous book shops, including but not limited to, HarperCollins, Amazon, Dymocks, Booktopia and Angus and Robertson.

With Dr Sara Gottfried as the Chief Medical Officer for Metagenics Institute, we are extremely proud and grateful we can leverage her immense clinical expertise for the betterment of clinical education and support.

Research

Bites

Ginger a novel strategy to battle cancer.

A recent review confirms the humble root, ginger may be a key player in the fight against cancer.3 The various active compounds in ginger (including gingerol, paradol, zingiberene and shagaol) have potential to inhibit cancer growth through modulating cell signaling pathways.

Predominantly antioxidant and anti-tumour

16

activity aids cancer management by impacting tumour suppressor genes, cell cycles, apoptosis, transcription factors, and angiogenesis. As a preventative measure for all patients or those at risk, spice up their treatment with health-promoting ginger.

Globe artichoke reverses fatty liver havoc.

Bitter digestive herb, globe artichoke has been shown to reverse structural changes in non-alcoholic fatty liver disease (NAFLD).4 A total of 100 individuals were randomised to receive either 600 mg of globe artichoke extract or placebo for 2 months and were

assessed with ultrasonography and pathology tests to determine response to treatment.

Outcomes of the study revealed a significant reduction in liver size and decreased in liver enzymes, alanine aminotransferase (ALT) and aspartate amino transferase (AST), correlating with reduced tissue fibrosis and liver regeneration. More than just a digestive, globe artichoke enhances liver repair amidst chronic NAFLD!

FOOD FOR THOUGHT

Do we need to defeat genes to beat obesity?

“The obese patient is not the villain in the story. Rather, the obese patient appears as the anonymous hero who tries to defeat their obesogenic genes in a hostile hypercaloric sedentary environment.”

- Prof Vidal-Puig and Prof Moukayed, 2018.1

Written by DANIELLE FAIRBROTHER Naturopath and Head of Marketing

I

n the modern world, obesity plagues our population causing great human sufferance, not to mention a $2 trillion annual burden on the economy.2 The natural response to this encumbrance is to find a vulnerable scapegoat to blame, and in the case of obesity, ‘genetics’ have become a popular target. However, doubt has been cast as to the extent by which genes influence obesity risk.

In 2005, 34 year old identical twins, Ruth and Mary, made a guest appearance on the Oprah Winfrey show. The episode exceeded its desired quota of ratings, while presenting an interesting scientific conundrum. Despite sharing identical genetic material, Mary was obese: weighing 190 kg, approximately 136 kg heavier than her sister Ruth, who weighed only 54 kg. From their early teens, Mary’s eating behaviours varied wildly from those of her sister Ruth, leading to the dramatic contrast seen on Oprah Winfrey’s couch over two decades later.

McPherson (or her male counterpart). To date, genome-wide association studies (GWAS) which test the correlation between single nucleotide polymorphisms (SNPs) across the entire genome and the obesity incidence in a sample population4 have identified over 100 different candidate genes, and 500 genetic loci+ that may link to adiposity traits (Figure 1).

This research has demonstrated a putative role for an individuals’ genetic architecture in their body weight – showing genes pre-dispose to obesity, or the opposing end of the spectrum thinness.5

The FATSO gene leads the charge The first ever genetic loci to be linked

to obesity in these genome wide discovery efforts, was the FTO (FaT mass and Obesityassociated) gene, which has since earned the nickname FATSO in the popular press. Since its discovery in 2007,7 FATSO has become the most studied and propagated fat gene, appearing on many of the weight-related SNP panels currently available. While every person

Identical twins Ruth and Mary appear on the Oprah Winfrey show in 2005.

Fat gene shaming 500

Weight loss after bariatric surgery Circulating leptin levels

Cumulative number of independent loci

Two years prior to Ruth and Mary’s television debut, we witnessed what was touted as the biggest breakthrough in medical history of our time – the Human Genome Project (HGP) announced that finally, after 13 years and 2.7 billion dollars invested, the first ever entire human genome had been sequenced.3* Overwhelming excitement ensued as we believed we’d unearthed the Holy Grail of medicine that would enable us to predict every individual’s unique disease risk, well before its onset, then offset that with truly personalised dietary and lifestyle advice, medical interventions and innovative, DNAbased therapies.

The genes that have since topped the charts in the scientific literature are largely related to the two leading causes of death worldwide, cancer and cardiovascular disease. However, obesity has also emerged as a key area of interest. Both medical professionals and commercial opportunists alike are desperate to name and shame genes that ‘cause’ obesity and obtain genomic direction on the specific diet an individual should eat, to most closely resemble the physique of Elle

Visceral and abdominal adipose tissue

400

Lean mass Body fat percentage Childhood obesity and BMI

300

Extreme and early onset obesity Overweight and obesity Waist-to-hip ratio (African)

200

Waist-to-hip ratio (Asian) Waist-to-hip ratio (European) BMI (African)

100

BMI (Asian) BMI (predominantly European)

0 Current Opinion in Genetics & Development

Figure 1: The cumulative number of independent genetic loci linked to specific adiposity traits such as Body Mass Index (BMI) (dark navy and purple), waist-to-hop ratio (red) and body composition (green) has grown considerably since the FTO gene was first identified in 2007.6

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FOOD FOR THOUGHT

possesses the FTO-gene, obesity risk is tied to SNPs that may occur at two specific alleles (Figure 2). Evidence suggests that those who carry homozygous SNPs at either of these alleles, are prone to disordered central (brain) regulation of food, reducing satiety, leading to poor food choices and greater energy consumption (as opposed to reducing energy expenditure).8 The consequence: an increased propensity for gaining fat. Various other genes are also now accumulating evidence of their involvement in body weight regulation. These include brain-derived neurotropic factor (BDNF), melanocortin 4 receptor (MC4r), neural growth regulator 1 (NEGR1) to name a few, and are now being keenly investigated for their mechanistic role in fat accumulation.

The sum of the parts and then some Given these documented examples, it is not unreasonable to draw a simple conclusion – the requirement for larger size jeans, is driven directly by our genes. While not completely inaccurate, before we race to implement SNP testing in all our overweight patients, this oversimplified statement is in need of qualification. Recall, every phenotype (i.e. the observable end product) is polygenic. It results from the convergence of multiple patterns and combinations of gene variants, some protective and some harmful. ‡ This means, even though someone carries FTO SNPs they could also carry protective genetic polymorphisms that counter its effects. What’s more, the human genome consists of more than 23,000 genes, with each gene possessing anywhere from several hundred to two million DNA bases (which are then paired!), allowing for an infinite amount of potential SNPs. Examining one gene SNP in isolation, or even a small panel of SNPs, is akin to examining the impact of a drop of water on two Olympic-sized pools combined.

With that context, it is not surprising that the majority of obesity loci identified seemingly exert a minor overall influence on body weight outcomes, accounting for a very small variation in obesity risk.9 Even the most characterised and quantified ‘fat gene,’ the FTO variants, exert a fairly modest increase in risk, equating

A T G

A T G

to a potential 1 to 3 extra kilos over the course of a lifetime. Some researchers have attempted to sum up the additive impact of multiple BMI-increasing alleles, computing a genetic risk ‘score’, however, their predictive accuracy is still considered insufficient for clinical diagnosis or treatment decision making.10

Genes are knotty by nature Deciphering the impact of our genes on body weight goes beyond their additive effects. It is further complicated by their pleiotropic effects – essentially the reverse description of polygenic. Just as multiple genes contribute to one phenotype, one gene can generate multiple phenotypes.

This provides further rationale as to why many of the ‘risky’ SNPs identified in GWAS studies at this stage are showing only feeble connections to the biology of body weight regulation.11 Overlay this with the phenomenon of antagonistic pleiotropy and epistasis and our genetic ‘crystal ball’ becomes even cloudier. Antagonistic pleiotropy is when the expression of a single gene causes competing effects, some of which are beneficial and some of which are detrimental to the fitness of an organism. For example, Roos and colleagues, discovered some of the genes that apparently increase body fat percentage, counterintuitively, also protect against cardiometabolic complications.12 § Epistasis describes the complex hierarchical relationships that exist between genes, whereby one gene may hide, mask or modify the visible output of another gene altogether.

No truer is the ancient Japanese proverb, ‘the whole is greater than the sum of its parts’ than when looking at the collective output of genes.

When we contemplate the interactions of polygenetics, pleiotropy and epistasis, all of a sudden A G T G one assessing patients for T G A C or two SNPs, seems lessC like examining a drop of Awater G T G in two Olympic pools, Gand C T C A more like a drop within the AtlanticAOcean.

Wild Type (normal)

A T G

G G

C A C

T

A T G

G G

C A C

T

A Wild Type (normal)

B

Unravelling this complexity may be feasible in the future, particularly if promises of artificial intelligence, machine learning and big data come into fruition, however as it stands today, we don’t have the tools at our disposal to make wholesale conclusions off genetic information alone.

With all of this said, it is well established that obesity, or specifically BMI, is highly heritable, with family, twin, and adoption studies reporting heritability estimates of 40% to 70%.13 No doubt obesity ‘runs in the family’ yet the early evidence evaluating the inherited nature of obesity report that genes contribute less than 2% to inter-individual BMI variation.14 This begs the question, what else is inherited that accounts for the difference?

We inherit more than genes and finances Up until 2015, it was always thought that the womb was sterile, and that every baby was born as a clean, microbe-free canvas. We now understand that our core microbiome, an even bigger source of genetic material than human DNA, begins to form in utero and is inherited from the mother, mirroring the composition of her gut, oral and vaginal microbiome. What’s more, the microbiome is now strongly implicated in obesity, with evidence suggesting it may exert an even greater influence than human genetics on adiposity traits such as waist circumference and waist-to-hip ratio.15 Interestingly, the A G G microbiome has also shown Tmore promise as T G C C A a means of personalising dietary approaches A for weight loss and cardiometabolic health G T G T G than the genome, according to innovative C A C research coming out of the Weizmann Institute in Israel. Published premier journal, A in Wild Typescience (normal) Cell, the seminal work led by Eran Segal and Eran Elinav tracked the dietary intake and blood glucose levels of over 800 subjects for a week. Two key conclusions emerged: one, A G T G given food that the glycaemic index of any T G C A C is not a set value, but a uniquely individual response; and two, that this individual response A G T G T is contingent on the person’s unique microbial G C T C characteristics.16 Whilst the evidence is still in its infancy, it certainly down plays the relative B Heterozygous

A T G

G G

C A C

T

A T G

G G

C T C

T

Heterozygous

C

G G

C T C

G G

C T C

Homozygous

Figure 2: The two FTO gene alleles that incur SNPs linked to obesity risk are labelled as rs9939609 and rs1558902. At each of these alleles, the normal gene A (i.e. wild-type) should have an adenine-base however in those with the SNP, the sequence isAaltered whereby adenine is replaced with a thiamine-base.

G G T G T G T T If this polymorphism is inherited from SNP and the inherent risks are greater.

Gboth the mother and the father then this is known as a homozygous G C A C

A T G

18 B

C T C

A T G

G G

C T C

Heterozygous

T

C

G G

Homozygous

C T C

T

T

T

FOOD FOR THOUGHT

Facts and Footnotes * Though the first draft of the human genome was presented in the year 2000, and is often quoted as the date we ‘cracked the genetic code’, the Human Genome Project was not officially declared as complete until 2003. + A locus (plural loci) in genetics is a fixed position on a chromosome, like the position of a gene or a marker. A variant of the similar DNA sequence located at a given locus is called an allele. ‡ Although, most clinical presentations are polygenic whereby each gene has only a slight influence overall, there are some more rare and serious conditions which many be monogenic – meaning they result from a single defective gene. Monogenic obesity is described as rare and severe early-onset obesity with abnormal feeding behavior and disordered endocrine function mainly due to mutations in genes of the leptin/melanocortin axis involved in food intake regulation (genes of leptin (LEP) and leptin receptor (LEPR), proopiomelanocortin (POMC), proconvertase 1 (PC1). § Not all instances of pleiotropy are straightforward. For example, in humans, the p53 gene directs damaged cells to stop reproducing, thereby resulting in cell death. This gene helps avert cancer by preventing cells with DNA damage from dividing, but it also suppresses the division of stem cells, which allow the body to renew and replace deteriorating tissues during ageing. ** Melanocortin 4 receptor (MC4R) is involved in the hypothalamic leptin-melanocortin signaling pathway and plays a key role in energy homeostasis. The majority of patients are carriers of heterozygous mutations in the MC4R gene which produces a less severe phenotype however rare homozygous carriers suffer MC4R deficiency which is characterised by severe obesity.

This is the most common form of monogenic obesity identified to date.

importance of the human genome in dietary responses. Cumulative data suggests the missing heritability of BMI could be owing to our microbes.

Epigenetics transcends generations In addition to inheriting our mother’s microbiome in utero, she also gifts us with her epigenetic footprint – the degree to which various genes are ‘turned up’ or ‘down’, ultimately affecting their activity. Epigenetics cannot alter the fact one carries the FTO variant as the genetic code remains hardwired, it does however modulate the translation of those genes, completely altering the phenotype of her offspring. The landmark study in this area involved the Agouti mice, whereby the expression of the agouti gene, which produces yellow fur and obesity, was altered by the diet fed to the mothers.17 Specifically, it was the maternal dietary influence over this gene, as opposed to the gene itself that dictated whether mice grew up to be yellow and fat, or brown and slim. These in utero effects, haven’t just been seen in mice, there have been some unintended human experiments as well.

The Quebec Ice Storm of 1998 was a devastating time that plunged more than 3 million Canadians into frigid darkness without electricity for as long as 45 days. Women who were pregnant during this natural disaster now have children that are almost 20 years old and present higher rates of various health disorders of which obesity is one.18 This is just one example of many studies which demonstrate the impact of maternal exposures on genetic expression of the offspring. As TIME Magazine headlines in 2010, when the science of epigenetics was taking off – this explains “why your DNA isn’t your destiny… [and] how the choices you make can change your genes and those of your kids.” Human

epigenetic machinery is highly vulnerable (especially in utero), reacting to environmental cues coming from the mother’s exposome.

In particular, maternal stress trauma, poor nutrition and toxin exposure during pregnancy have been linked to increased incidence of obesity.19 Interestingly, this environmental exposure usually continues past the in utero period and represents another factor typically inherited from our parents, outside of their genes – their lifestyle and environment.

One fact that has clearly emerged during the last two decades of genetic research, even those genes dubbed as ‘bad’ can be relatively benign until they are exposed to a hostile environment. In the case of obesity that usually entails a sedentary, obesogenic diet and lifestyle characteristic of the modern world.

Diet and exercise: the one-two punch When you consider the combined impact of microbial genes and environmental influences over gene expression, the body of water expands, and one genetic SNP may be as relevant as a drop of water within all of the oceans on Earth. The good news is that these more important obesogenic influences are more malleable and plastic than the hardwired gene coding, and are particularly susceptible to two generic interventions – healthy diet and physical activity. To use the FTO variant as the poster child once again, not only is the risk of carrying these SNPs modest at best, it can be easily mitigated with generalised dietary and lifestyle interventions. One meta-analysis combining the data of more than 218,000 adults concluded that adequate physical activity negated any risk of this particular variant,20 and, another large meta-analysis of over 200,000 adults from 45 studies, found that having the ‘genetic predisposition’ for obesity did not reduce participants ability to lose weight.21

Dietary studies have presented similar findings, and even found that FTO SNP carriers actually responded more favourably, achieving greater weight loss with dietary interventions such as a high protein or Mediterranean diet than their non-SNP counterparts!22 This implies that while they might gain weight more easily under hostile conditions (i.e. a poor diet) they also lose weight more easily under healthful conditions. This isn’t just true for FTO gene.

Recently, Danish researchers decided to study the degree to which genetics altered the response to dietary and lifestyle interventions, examining 754 overweight children and adolescents. The participants carried 15 genetic variants linked to obesity, yet their genetic profile did not impact their ability to lose weight when following the series interventions except for the rare gene MC4R.23 ** One of the authors, Jens-Christian Holm, Head of the Children’s Obesity Clinic at Holbæk Hospital succinctly quoted “‘large parts of the population believe that when you have problematic genes it is game over. That is why it is very important we send a clear message that even though you have a genetic sensitivity, this treatment can help people. We have discovered that it does not matter whether the children and adolescents have an increased genetic risk score or not. They can respond to treatment just as well.” Diet and exercise will help people stay lean despite their genetic signature.

The fate of body weight As Ruth and Mary clearly demonstrated on Oprah’s couch all those years ago, genes do not completely dictate the fate of body weight. In the absence of machine learning and complex algorithms that can dictate how genes, epigenetics, microbial DNA, diet and lifestyle all interact, the exact cause of Ruth’s disordered eating and weight, and the exact contribution of each to the risk of any of our patients, remains as yet unknown.

That said, one thing that decades of research has continued to confirm is that a healthful, calorie-controlled diet and physical activity are the panacea for all weight woes.

19

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