Dr. Laura: Menopause-could probiotics be the answer?

The microbiome shows distinct differences in pre and post menopausal women, a 2019 study reports.

The change in microbiome could help us better understand the reasons for health decline in many post-menopausal women. The presence of estrogen protects against cardiovascular, metabolic disease and bone health. Now mounting evidence shows how the gut microbiota affects estrogen metabolism levels. It is unclear if the post-menopausal decline in estrogen is directly related to the change in diversity of the microbiome. We do know that estrogen hold some regulatory capacity in the immune system and more than 70% of the immune system resides in the gut.

Bone health

Additionally, probiotics can help in bone mineral matrix as the microbes in the gut are responsible for secreting a host of metabolites into the blood stream. Aging women tend to have more Tolumonas microbes. These particular bacterium produce toluene which can reduce bone mineral density.

Some evidence that compares the microbiome of the pre and post menopausal women showed that the bacteria seemed to be more satisfied in the earlier years and tend to compete with each other for nutrient substrates in later years. A decline in estrogen after menopause could increase the bacterial demand for calcium.

Cardiovascular health

Post-menopausal women have a microbiome that produces more cysteine and homocysteine. These components absorb across the small intestine into the blood stream and pose as risk factors for cardiovascular disease. You can take a lab test to measure you homocysteine levels.

Immune health

It is important to uphold a diverse microbiome to keep the immune system healthy and strong. Older women have higher levels of E.coli and Bacteroides and lower levels of bacteria in the Firmicutes family. Younger women have more Roseburia and less Parabacteroides. The ratios of these microbes in older women links to metabolic and endocrine disorders.

Probiotics for anti-aging

This might be all Greek to you and me, (actually the names of all these critters are in Latin), but the take away is pretty cool. Some of the difference found between pre and post menopausal individuals may provide leadership into the field of anti-aging with probiotic therapy.

References

Hui ZhaoJuanjuan ChenXiaoping LiQiang SunPanpan QinQi Wang Compositional and functional features of the female premenopausal and postmenopausal gut microbiota. First published: 05 July 2019 https://doi.org/10.1002/1873-3468.13527

Dr. Phil Shares: Lifting Weights Could Lower Your Risk of Type 2 Diabetes

Lifting Weights Could Lower Your Risk of Type 2 Diabetes

A whopping 30 million North Americans have been diagnosed with Type 2 diabetes — and more than 84 million more have higher than normal blood glucose levels (called prediabetes) and are at risk for developing the disease. Obesity is the leading risk factor for developing Type 2 diabetes.

The rising rates of Type 2 diabetes also mean increased potential for developing serious health complications ranging from heart disease and stroke to vision loss and premature death. Exercise could be the antidote.

THE IMPACT OF EXERCISE ON TYPE 2 DIABETES

Several studies have found exercise can prevent or delay the onset of Type 2 diabetes; some research has shown a 58% risk reduction among high-risk populations. While much of the research has looked at the impact of moderate-to high-intensity cardiovascular exercise, a new study published in Mayo Clinic Proceedings examined the potential impact of strength training on Type 2 diabetes risk. The data showed building muscle strength was associated with a 32% lowered risk of developing Type 2 diabetes.

Study co-author Yuehan Wang, PhD, notes resistance training may help improve glucose levels by increasing lean body mass and reducing waist circumference, which is associated with insulin resistance — and achieving results doesn’t require lifting heavy weights or spending countless hours in the gym.

“Our study showed that very high levels of resistance training may not be necessary to obtain considerable health benefits on preventing Type 2 diabetes,” Wang says. “Small and simple resistance exercises like squats and planks can benefit your health even if you don’t lose any weight.”

Think twice before abandoning the treadmill or elliptical trainer for the weight room, advises Eric Shiroma, ScD, staff scientist at the National Institute on Aging.

As part of a 2018 study, Shiroma and his colleagues followed more than 35,000 healthy women for 14 years and found women who incorporated strength training into their workouts experienced a 30% lowered risk of Type 2 diabetes but women who also participated in cardiovascular activities experienced additional risk reduction.

“When comparing the same amount of time in all cardio, strength [training] or a combination, the combination had the most Type 2 diabetes risk reduction,” Shiroma explains.

THE BOTTOM LINE

Researchers are still unclear about which type of exercise could have the biggest impact on reducing your risk. Wang suggests erring on the side of caution and following a workout regimen that blends both pumping iron and heart-pumping cardio, explaining, “Both strength training and cardiovascular aerobic training are important for the prevention of Type 2 diabetes.”

The biggest takeaway, according to Shiroma, is any amount of exercise is beneficial for reducing Type 2 diabetes risk so do pushups or take a walk around the block as long as you get moving.

by Jodi Helmer

Shared by Dr. Phil McAllister @ Forward Health Guelph

Dr. Laura: How Sugar Ages the Brain

Vulnerable populations with long term unmanaged blood sugar levels are subject to brain atrophy (shrinkage) and accelerated brain changes including memory loss and cognitive decline.

Memory Lapses?

Vulnerable populations with long term unmanaged blood sugar levels are subject to accelerated brain changes including memory loss and cognitive decline. 

Who’s most at risk?

Most at risk are those with Diabetes type I and II monitor sugar regularly and those with metabolic syndrome or cardiovascular disease. 

But that’s not all. 

Anyone with long term fluctuating blood sugar levels could be at risk for cognitive decline. So those with chronic stress are also at risk. Stress elevates cortisol, which subsequently activates sugar into the blood stream. This is really helpful when we need the energy to physically run from the tiger.  However, in our day in age, the tiger is more likely to be the boss, the lack of sleep, the poor diet, or the overscheduled.  Stress, namely long-term cortisol release, affects the microbiome. Certain drugs like antibiotics and oral birth control pills can also change the microbiome. Shifts in populations of gut bacteria can evidently impact blood glucose regulation. Overgrowth of candida can make us crave sugars and leave us in a state of flux or what we have now termed “hangry”. 

If you are the hangry type, you likely have issues with blood sugar. 

A state of blood sugar surges and crashes overtime will lead to unfortunate hippocampus affects, namely sugar induced shrinkage and memory challenges. 

Those at risk:

  • long term fluctuating blood sugar levels
  • history of oral birth control use
  • history of antibiotic use
  • diabetic patients on metformin
  • elevated cortisol
  • chronic stress
  • poor diet
  • lack of moderate regular exercise
  • disrupted sleep patterns

What’s a healthy blood sugar level?

Guidelines for healthy levels are subject to some interpretation, however from a functional medicine point of view, HbA1c should be between 4.6 and 5.3% and fasting blood sugar levels are healthiest around 4-6mmol/L. Note that those with red blood cell disease like sickle cell anemia, which change the shape of the blood cell, HbA1c is not a reliable marker and other markers like triglycerides, and fasting blood sugar levels must be taken into account. 

Protect your brain

Protect memory and cognition with adequate blood supply, high levels ofanthocyanins, appropriate levels of B vitamins, omega-3 fatty acids and a diet low in sugar and high in fibre, protein and healthy fats. Caution with drugs like metformin, which help regulate blood sugar in diabetics and is associated with cognitive decline. Apparently, this could be due to a number of factors, and not just the drug directly; it is therefore important to monitor B2 (riboflavin), B6, B12 when on metformin. 

It is important to include in the diet:

  • high levels of anthocyanins
  • plant powers found in dark blue and purple fruits and vegetables
  • consistent intake of B-vitamins 
  • egg yolks, red meat, liver, clams, mussels, avocados and dark leafy greens
  • daily dose of omega-3 essential fatty acids
  • cold water fatty fish like salmon and sardines
  • flax, hemp and walnut

Is diet alone enough?

Is diet enough to keep up with the demands of cognitive decline? It is difficult to know as diets of many individuals need to be followed for years and it is difficult to control what people eat on a daily basis for any length of time. First and fore most get what you can from the diet, yes, this is critical as the body knows best how to get nutrients from food. Insulin sensitivity is an important factor in blood glucose regulation and a short-term keto diet and or fasting is proven to be effective method to reset it. 

Reduce the risk factors as indicated above and get help to re-set the microbiome. That means create a sleep routine where you go to bed and wake up at the same time every night. Move your body every day for about 30 minutes. It means to have space in the day that is not filled with tasks and demands. Take appropriate supplements where diet falls short or medications deplete. 

Memory and cognition decline over time. It doesn’t happen overnight. So too should your changes and lifestyle reflect a long-term plan. If you feel you need help, Naturopathic Doctors are trained in lifestyle and laboratory analysis, diet, nutrition and nutraceuticals. 

Dr. Laura M. Brown, ND is a registered naturopathic doctor with a functional medicine approach.  She has advanced training in pharmaceuticals, is a certified HeartMath Practitioner and a Certified Gluten Free Practitioner  and holds the designation of ADAPT Trained Practitioner from Kresser Institute, the only functional medicine and ancestral health training company.

References:

Cui X, Abduljalil A, Manor BD, Peng CK, Novak V. Multi-scale glycemic variability: a link to gray matter atrophy and cognitive decline in type 2 diabetes. PLoS One. 2014;9(1):e86284. Published 2014 Jan 24. doi:10.1371/journal.pone.0086284

Zhao X, Han Q, Lv Y, Sun L, Gang X, Wang G. Biomarkers for cognitive decline in patients with diabetes mellitus: evidence from clinical studies. Oncotarget. 2017;9(7):7710–7726. Published 2017 Dec 14. doi:10.18632/oncotarget.23284

Dr. Laura: Why do processed foods get such a bad wrap?

Advanced Glycated End products

AGES– Advanced Glycated End products area product of food processing. AGEs appear to stimulate chronic low-grade inflammation and promote oxidative stress and affect the pancreatic beta cell function leading to the development of insulin resistance. Stop AGE diets in animal models and diabetes stops.

Bad Fats

Fats– Not all are created equal! Processed foods use trans fats to prolong shelf life, saturated fats because they are cheap and tasty. Transfats and arachadonic acids create inflammation in the body. This increases risk for plaques in the vascular system, increases cholesterol and ultimately blood pressure. In contrast, when healthy fats like omega 3 fatty acids (aka high quality fish oil) the inflammation markers go down, the cell is better able to perform its function. Since every cell has a phospholipid bilayer. This means that every cell’s skin is made of fat. When fat is of a fluid nature, nutrients are able pass in and out more effectively and the cell’s function is optimized.

Food Dyes

Dyes–The processed food industry uses food dyes to add colour to colourless foods, to enhance colour and to avoid colour loss due to environmental elements and to preserve consistency when there are variations in the colour of food. Food dyes are know to cause inattention, hyperactivity, irritability, temper tantrums or trouble sleeping.

Sugars

Sugar & high fructose corn syrup. Most processed foods have some sugar added including soda pop, breads, cereals, yogurts, processed meats, soups and condiments. High-sugar diets may make a significant contribution to cardio-metabolic risk.  High fructose corn syrup, when digested by the body produces reactive carbonyls, which creates tissue damage. Countries using high-fructose corn syrup had rates of diabetes that were about 20% higher than countries that didn’t mix the sweetener into foods, even when total sugar and total calories remain the same.

Salt

Salt– Processed foods use salt to help preserve it and for added flavour. The amount of salt in restaurant and packaged foods are the main culprits in the Western diet, not the salt added to home-prepared whole foods.  Research shows that the average North American consumes 4000mg sodium per 2000kcal diet. This is almost twice as much as the 2300mg/day recommend by some health experts. If the amount reduces even to 2700mg/day, a 5mmHg smaller rise in systolic blood pressure would be noted in those 25-55 years of age. This results in an estimated 150,000 lives saved from death due to cardiovascular events. The kicker is, if not getting annual checkups, often the first sign of high blood pressure, is a deadly heart attack.

White Flour

White flour  – Without the fibre, white flour easily breaks down quickly into simple carbohydrates, which is essentially sugar to the body. Processed foods are full of white flour. The fast breakdown quickly elevates blood sugar, induces insulin release and quickly and causes cravings for more sugar to restore blood sugar levels. The cycle easily repeats itself as quick carbs are continually fed into the body. Over time and continued food abuse, the insulin that works diligently to get the sugar into the cells, becomes less effective, the sugar stays in the blood stream and the person is now experiencing high blood sugar levels and insulin resistance… a path well travelled to the diabetes destination.

Dr. Phil Shares: Not Taking a Multivitamin? Here Are the Top 5 Reasons You Should Be

You try to eat well to feel good and stay healthy. While it’s optimal to get your nutritional needs from the foods you eat, it’s not always possible. There is conflicting information out there on the benefits of supplements, but the Dietary Guidelines for Americans 2015-20201 say that supplements may be useful for providing the nutrients you may be lacking from diet alone.

Still on the fence? Consider these top five reasons to add a multivitamin to your daily regimen.

  1. Healthy aging. As we get older, our bodies have a harder time absorbing nutrients from food. The National Institute on Aging notes that starting around age 50, people begin to require increased amounts of certain vitamins and minerals.1 In fact, according to a study published in the June 2009 issue of the American Journal of Clinical Nutrition, researchers found that taking a daily multivitamin & mineral supplement may help improve micronutrient deficiencies associated with aging.3
  2. Making up for eliminated food groups. While some people have to cut certain foods like nuts or gluten out of their diets due to allergies, many eliminate particular foods or food groups from their diet voluntarily. This can cause vitamin deficiencies that would be helped with a multivitamin.
    Trying a paleo diet? You might risk a shortage of calcium or vitamin D by eliminating dairy or grains. Cutting back on red meat? A multivitamin will replace the iron and B12 you would normally get from diet.
  1. Getting the RDAs you’re not getting from food.You’ve probably heard that the typical Western diet doesn’t include nearly enough daily fruits and vegetables. As part of that, you don’t always get the vitamins those natural foods supply. Supplementing with a multivitamin containing phytonutrients from fruit- and vegetable-derived ingredients may help. In addition, it’s important to keep in mind that RDA levels are set to prevent nutrient deficiencies. But there’s a wide range between taking enough vitamin C to avoid scurvy and the optimal amount you can benefit from.
  2. Getting that extra energy to get through the day. In today’s “go-go-go” society, one of the top complaints is a general lack of energy. Instead of reaching for that third cup of coffee, remember that your cells require certain vitamins and minerals to power your busy life; especially if you’re not getting a full eight hours of sleep or eating a balanced diet, a multivitamin can help provide the nutrients you need to feel energetic throughout the day.4
  3. Managing stress. Daily life stressing you out? You’re not alone. But vitamins and micronutrients play a significant biochemical role in improving your brain’s cognitive processes, and studies have shown that a daily multivitamin—particularly one with high doses of B vitamins—can help to reduce stress and support a healthy mood.5

Ready to add a daily multivitamin to your diet? Be sure to check with your healthcare practitioner to see if he or she has a recommendation and to ensure that any medications you’re currently on won’t interfere with their effectiveness.

Shared by Dr. Phil McAllister @ Forward Health Guelph

Dr. Phil Shares: Menopause Belly: Why Fat Accumulates & How to Tackle It?

 

Many women notice after age 45 that fat seems to accumulate readily at the waist. There are even terms for it, like menopause belly, muffin top, or “meno-pot.” What does the science tell us about menopausal belly fat and how to get rid of it? What are the hormonal drivers and are they amenable to change with personalized lifestyle medicine? Certainly belly fat, specifically subcutaneous and visceral abdominal fat, increases during menopause,1-3 when the changing hormonal environment can bring with it a remodeling of fat storage patterns. Abdominal fat, especially visceral fat, is biochemically different and more metabolically active than fat stored in other areas, secreting more pro-inflammatory cytokines and adipokines.4 That means preventing or reversing belly fat is not just a vanity project, it’s a meaningful step in managing a woman’s overall health, as abdominal fat has been consistently linked with insulin resistance, impaired glucose control, and overall higher cardiometabolic and breast cancer risk. Practitioners are often asked ‘How can I get rid of menopausal belly fat?’, and it is important to remember that effective management is multifaceted – encompassing an understanding how changes in sex steroids interact with other endocrine systems and also with lifestyle choices, and recognizing the best time to implement a lifestyle medicine approach is in the years before a woman’s final menstrual period.

The changing hormonal environment

A robust understanding of the hormonal changes associated with perimenopause and menopause can guide women toward effective intervention. Here are the top five hormonal changes associated with the menopausal transition.

  • Changes in estrogen and estrogen dominance: Menopause is often framed simply as the loss of estrogen, but the road from pre- to post-menopausal estrogen levels is not necessarily smooth. Although loss of estrogen itself is linked with increasing abdominal fat,2,3 paradoxically the estrogen dominance that occurs in perimenopause and that may continue into menopause is seen clinically as a culprit in expanding abdominal fat mass.5 Between age 35 and 45, most women are beginning to run low on ripe eggs and experience hormonal changes linked with advancing reproductive age.6 During this time reduced progesterone coupled with high and erratic estrogen occurs.6,7 Estrogen declines but is in relative excess to progesterone. This is the definition of estrogen dominance: having a progesterone level that’s less than 100X the level of estrogen, creating an imbalance in the estrogen-progesterone partnership and essentially an inadequate level of progesterone to keep estrogen in check. Local estrogen production in adipose tissue can also contribute to estrogen dominance during this time. For example, aromatase enzymes, responsible for converting androgens to estrogens, are more active in visceral adipose tissue of post-menopausal women in response to cortisol.8

 

  • Cortisol: Dysregulation of the HPA axis and cortisol excess can manifest as increased central and visceral fat mass and metabolic disturbances such as insulin resistance.9,10 Increased production of cortisol,11 and conversion of cortisone (inactive) to cortisol (active) has been described in post-menopausal women,12 indicating that increased cortisol synthesis and conversion could contribute to metabolic dysfunction in these women. Cortisol is regulated in part by sex steroids, and estrogen down-regulates the expression and activity 11β-HSD1, the enzyme involved in converting inactive cortisone to active cortisol13 – so higher estrogen, lower 11β-HSD1 and less active cortisol formed. Declining estrogen levels during menopause can have a knock-on effect on cortisol formation, and 11β-HSD1 has been shown to be upregulated particularly in visceral fat in post-menopausal compared with pre-menopausal women. 1,11,12 As well as contributing directly metabolic dysfunction, higher cortisol can feed back to hormonal environment and contribute to estrogen dominance occurring at this time through cortisol-induced aromatase activity.8,14

 

  • Insulin: Fat cells accumulating in the abdomen is linked with insulin resistance. The pro-inflammatory cytokines produced by abdominal fat interferes with insulin signaling.15 This results in insulin resistance where cell response to insulin is lost, which creates a cycle where greater production of insulin is required to manage blood glucose levels. Insulin is a gatekeeper of metabolism, and rising insulin levels can set off a chain reaction that ultimately leads to a cycle of weight and abdominal fat gain. Insulin can lower production of sex hormone binding globulin (SHBG) in the liver.16,17 Lower SHBG results in greater free androgens and estrogens in circulation, and is linked with visceral fat and insulin resistance in menopausal women.18,19 In addition, insulin resistance can have a knock-on effect on leptin, insulin’s cousin.

 

  • Leptin: Leptin is the put-down-your-fork hormone, the one that tells you when you are full.20 Elevated insulin levels eventually lead to elevated leptin, which despite what you may think, does not mean you are more likely to put down your fork and stop eating. Instead, consistently elevated leptin levels lead to a dysfunction of leptin receptors and they stop sending signals to the brain to tell you to stop eating – this is called leptin resistance.21 The mechanisms driving leptin-resistance are complex, but high intakes of refined carbohydrates have linked with its development.22

 

  • Thyroid hormones: Thyroid hormones, which regulate how quickly we burn calories and maintains our metabolism, can becomes unbalanced with age, a trend that has been labeled ‘thyropause’. If the thyroid becomes underactive, this can lead to symptoms including weakness, fatigue, and weight gain.23

What can be done?

One of the biggest myths in women’s health is that once hormones change with menopause, abdominal adiposity is immovable – however addressing modifiable hormones such as cortisol and insulin in the following ways can have an impact.

  • Make foundational changes to dietary intake. When evaluating diet, consider factors that influence insulin levels, such as high carbohydrate intakes or intake of refined carbohydrates which require greater insulin response to manage spikes in plasma glucose. Remove inflammatory or trigger foods, as inflammation can contribute to insulin resistance.31 Add in foods rich in antioxidants which promote detoxification. Eliminate alcohol which robs you of deep sleep and lowers metabolism by more than 70% for 24 hours. Choosing when to eat during the day can also make a positive impact to insulin levels and insulin sensitivity. Time-restricted feeding (TRF) protocols, a type of intermittent fasting, where food is consumed during a limited number of hours per day (often 6 or 8) has been shown to reduce body weight and abdominal fat32 and improve insulin sensitivity even without weight loss.33

 

  • Add more movement to the day. Sitting is like the new smoking. Approximately 35 chronic diseases and conditions are associated with sedentariness, and sedentary behavior makes people more prone to gain body fat.24 High intensity interval training (HIIT) is effective at reducing abdominal and visceral adiposity, as well as improving insulin sensitivity and building muscle.25,26 Studies in post-menopausal women show that HIIT training results in greater abdominal and visceral fat mass loss compared to continuous exercise programs (where heart rate was maintained at a constant level)27,28 showing that HIIT is a time-efficient strategy for improving central obesity in this population. In addition to HIIT programs, practicing yoga can be recommended for menopausal women, showing significant reductions in menopausal symptoms.29 In broader populations, interventions that included yoga asanas were associated with reduced evening and waking cortisol levels, as well as improved metabolic symptoms.30

 

  • Support reparative sleep. A primary step to losing belly fat is to get enough sleep and to make it quality sleep. Epidemiological studies have repeatedly shown links between sleep duration and the risk of obesity and central adiposity.34 People sleeping 7-8 hours/night night have been shown to accumulate less visceral fat mass than those sleeping for ≤6 hours/night.35 Sleep debt leads to changes in leptin and other hormones related to satiety, greater feelings of hunger, dietary indiscretion and poor food choices, as well as reduced physical activity and insulin resistance.34 In other words, getting that solid sleep needs to be a priority. As well as sleep quantity, sleep quality has to be considered, as poorer sleep quality is associated with higher visceral fat mass.36 Subjective poor sleep quality is linked with altered cortisol response37 and insulin resistance in postmenopausal women.38

by Sara Gottfried, MD and Annalouise O’Connor, PhD

Shared by Dr. Phil McAllister @ Forward Health Guelph

Citations

  1. Yamatani H et al. Association of estrogen with glucocorticoid levels in visceral fat in postmenopausal women. Menopause. 2013;20(4):437-442.
  2. Shen W et al. Sexual dimorphism of adipose tissue distribution across the lifespan: a cross-sectional whole-body magnetic resonance imaging study. Nutr Metab (Lond). 2009;6:17.
  3. Lovejoy JC et al. Increased visceral fat and decreased energy expenditure during the menopausal transition. Int J Obes (Lond). 2008;32(6):949-958.
  4. de Heredia FP et al. Obesity, inflammation and the immune system. Proc Nutr Soc. 2012;71(2):332-338.
  5. Prior JC. Progesterone for symptomatic perimenopause treatment – progesterone politics, physiology and potential for perimenopause. Facts Views Vis Obgyn. 2011;3(2):109-120.
  6. Hale GE et al. Hormonal changes and biomarkers in late reproductive age, menopausal transition and menopause. Best Pract Res Clin Obstet Gynaecol. 2009;23(1):7-23.
  7. Hale GE et al. Endocrine features of menstrual cycles in middle and late reproductive age and the menopausal transition classified according to the Staging of Reproductive Aging Workshop (STRAW) staging system. J Clin Endocrinol Metab. 2007;92(8):3060-3067.
  8. McTernan PG et al. Glucocorticoid regulation of p450 aromatase acitivty in human adipose tissue: gender and site differences. J Clin Endocrinol Metab. 2002;87(3):1327-1336.
  9. Paredes S et al. Cortisol: the villain in metabolic syndrome? Rev Assoc Med Bras (1992). 2014;60(1):84-92.
  10. Incollingo Rodriguez AC et al. Hypothalamic-pituitary-adrenal axis dysregulation and cortisol activity in obesity: a systematic review. Psychoneuroendocrinology. 2015;62:301-318.
  11. Li S et al. Effects of menopause on hepatic 11β-hydroxysteroid dehydrogenase type 1 actvity and adrenal sensitivity to adrenocorticotropin in healthy non-obese women. Gynecol Endocrinol. 2011;27(10):794-799.
  12. Andersson T et al. Tissue-specific increases in 11β-hydroxysteroid dehydrogenase type 1 in normal weight postmenopausal women. PLoS One. 2009;4(12):e8475.
  13. Andersson T et al. Estrogen reduces 11β-hydroxysteroid dehydrogenase type 1 in liver and visceral, but not subcutaneous, adipose tissue in rats. Obesity (Silver Spring). 2010;18(3):470-475.
  14. McTernan PG et al. Gender differences in the regulation of P450 aromatase expression and activity in human adipose tissue. Int J Obes Relat Metab Disord. 2000;24(7):875-881.
  15. Castro AV et al. Obesity, insulin resistance and comorbidities? Mechanisms of association. Arq Bras Endocrinol Metabol. 2014;58(6):600-609.
  16. Plymate SR et al. Inhibition of sex hormone-binding globulin production in the human hepatoma (Hep G2) cell line by insulin and prolactin. J Clin Endocrinol Metab. 1988;67(3):460-464.
  17. Loukovaara M et al. Regulation of production and secretion of sex hormone-binding globulin in HepG2 cell cultures by hormones and growth factors. J Clin Endocrinol Metab. 1995;80(1):160-164.
  18. Davis SR et al. The contribution of SHBG to the variation in HOMA-IR is not dependent on endogenous oestrogen or androgen levels in postmenopausal women. Clin Endocrinol (Oxf). 2012;77(4):541-547.
  19. Janssen I et al. Testosterone and visceral fat in midlife women: the Study of Women’s Health Across the Nation (SWAN) fat patterning study. Obesity (Silver Spring). 2010;18(3):604-610.
  20. Klok MD et al. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obes Rev. 2007;8(1):21-34.
  21. Engin A. Diet-induced obesity and the mechanism of leptin resistance. Adv Exp Med Biol. 2017;960:381-397.
  22. Harris RBS. Development of leptin resistance in sucrose drinking rats is assocated with consuming carbohydrate-containing solutions and not calorie-free sweet solution. Appetite. 2018;132:114-121.
  23. Diamanti-Kandarakis E et al. Mechanisms in endocrinology: aging and anti-aging: a combo-endocrinology overview Eur J Endocrinol. 2017;176(6):R283-R308.
  24. Levine JA. Sick of sitting. Diabetologia. 2015;58(8):1751-1758.
  25. Boutcher SH. High-intensity intermittent exercise and fat loss. J Obes. 2011;2011:868305.
  26. Maillard F et al. Effect of high-intensity interval training on total, abdominal and visceral fat mass: a meta-analysis. Sports Med. 2018;48(2):269-288.
  27. Maillard F et al. High-intensity interval training reduces abdominal fat mass in postmenopausal women with type 2 diabetes. Diabetes Metab. 2016;42(6):433-441.
  28. Nunes PRP et al. Effect of high-intensity interval training on body composition and inflammatory markers in obese postmenopausal women: a randomized controlled trial. Menopause. 2018;Oct 1.
  29. Cramer H et al. Yoga for menopausal symptoms-a systematic review and meta-analysis. Maturitas. 2018;109:13-25.
  30. Pascoe MC et al. Yoga, mindfulness-based stress reduction and stress-related physiological measures: a meta-analysis. Psychoneuroendocrinology. 2017;86:152-168.
  31. Caputo T et al. From chronic overnutrition to metainflammation and insulin resistance: adipose tissue and liver contributions. FEBS Lett. 2017;591(19):3061-3088.
  32. Gabel K et al. Effects of 8-hour time restricted feeding on body weight and metabolic disease risk factors in obese adults: a pilot study. Nutr Healthy Aging. 2018;4(4):345-353.
  33. Sutton EF et al. Early time-restricted feeding improves insulin sensitivity, blood pressure, and oxidative stress even without weight loss in men with prediabetes. Cell Metab. 2018;27(6):1212-1221.e3.
  34. Koren D et al. Role of sleep quality in the metabolic syndrome. Diabetes Metab Syndr Obes. 2016;9:281-310.
  35. Chaput JP et al. Change in sleep duration and visceral fat accumulation over 6 years in adults. Obesity (Silver Spring). 2014;22(5):E9-12.
  36. Sweatt SK et al. Sleep quality is differentially related to adiposity in adults. Psychoneuroendocrinology. 2018;98:46-51.
  37. Huang T et al. Habitual sleep quality and diurnal rhythms of salivary cortisol and dehydroepiandrosterone in postmenopausal women. Psychoneuroendocrinology. 2017;84:172-180.
  38. Kline CE et al. Poor sleep quality is associated with insulin resistance in postmenopausal women with and without metabolic syndrome. Metab Syndr Relat Disord. 2018;16(4):183-189.

 

Sara Gottfried, MD

Sara Gottfried, MD is a board-certified gynecologist and physician scientist. She graduated from Harvard Medical School and the Massachusetts Institute of Technology and completed residency at the University of California at San Francisco. Over the past two decades, Dr. Gottfried has seen more than 25,000 patients and specializes in identifying the underlying cause of her patients’ conditions to achieve true and lasting health transformations, not just symptom management.

Dr. Gottfried is the President of Metagenics Institute, which is dedicated to transforming healthcare by educating, inspiring, and mobilizing practitioners and patients to learn about and adopt personalized lifestyle medicine. Dr. Gottfried is a global keynote speaker who practices evidence-based integrative, precision, and Functional Medicine. She has written three New York Times bestselling books: The Hormone Cure, The Hormone Reset Diet, and her latest, Younger: A Breakthrough Program to Reset Your Genes, Reverse Aging, and Turn Back the Clock 10 Years.

Annalouise O’Connor, PhD, RD

Dr. Annalouise O’Connor is the R&D Manager for Therapeutic Platforms and Lead for Cardiometabolic and Obesity platforms at Metagenics. Her role involves research coordination, as well as developing formulas for targeted nutrition solutions and programs to assist practitioners in the optimal management of their patients’ health. Annalouise trained as an RD and worked in clinical and public health settings. Dr. O’Connor completed her PhD in the Nutrigenomics Research Group at University College Dublin (Ireland) and postdoctoral work at the UNC Chapel Hill Nutrition Research Institute.

 

Dr. Phil Shares: Staying Keto over the Holidays

It’s the most wonderful time of the year, but for those following a diet, the holidays may stir up stress and anxiety around food. The ketogenic diet is not the most “social” diet, but there are ways to stick to it, even in the most daunting of times, such as holiday celebrations.

If you can’t eat keto, at least aim for low-carb

Your holiday party may not be stocked full of keto-friendly foods, but there is a high probability that you can nibble on some low-carb options. The cheese platter is, more often than not, a pretty safe bet for cheese (of course!), but also for other low-carb foods such as nuts and meats. Just stay clear of candy-coated nuts, dried fruits, and cured meats you suspect may have added sugar!

Another low-carb holiday party go-to is the veggie platter. Lucky for you, this usually gets the least attention by guests, thereby giving you full access to it. Stick to the low-carb vegetables options such as broccoli, cauliflower, celery, and cucumber. If your event is serving dinner, opt for the meats or any salads (without sugar-loaded dressings), and low-carb vegetables. Things to stay away from are the mashed potatoes, any bread/pastry-like foods, sauces, and, of course, the sweets. Sticking with low-carb as opposed to ditching the diet completely will make transitioning back into ketosis much easier.

Prepare for success and give yourself options

If you are uncomfortable not knowing what food options will be available at your holiday gathering, prepare some food in advance. Better yet, prepare a keto-friendly dish to share with everyone! Take a high-fat dip to pair with that veggie platter and a salad dressing you can pour on any dry salads to avoid sugary dressings. You can also pack some snacks such as high-fat nuts (e.g. macadamia nuts) to graze on throughout the evening. Additionally, medium-chain triglyceride (MCT) oil is a great tool for ketogenic living. Fill a small jar with MCT oil to take with you and use on any dish or in beverages. MCTs are highly ketogenic and have even been shown to increase ketone production without carbohydrate restriction.1

The popularity of the ketogenic diet has made it simple to find recipes that anyone can enjoy. Consider making a ketogenic dessert to bring and share so you can “indulge” too, while also preventing you from caving into the temptations of sugar-laden treats.

Stay positive and remember your “why”

It can be difficult to gain the support of those around you when your dietary choices are perceived as something as radical as a ketogenic diet may seem to some. You may even be tempted to ditch the diet for the sake of your peers or those family members who just won’t back down from having you try “just one bite.” Be prepared to explain to others what the ketogenic diet is and why you follow it. Remember that there is no one-size-fits-all diet, and it is perfectly fine to have different views from others. Just stay true to yourself, remember your “why,” and stay positive, because there is nothing worse than engaging in a debate over food choices!

Tips for alcohol

Alcohol isn’t generally conducive to living a ketogenic lifestyle, and if you have no problem abstaining from it completely, that is your best option. If having a drink in your hand makes you feel more comfortable in a crowd, take club soda and sliced lemon with you; this will help you feel less segregated. With all this said, celebrations may be times when you can make exceptions (within reason). There are ways to enjoy a drink or two and stick to your goals; you just have to know what to look out for. For wines, opt for the driest you can find, white or red, and avoid sweet wines such as rosé. Most liquors are acceptable on their own or enjoyed with club soda or sugar-free beverages. Beers typically contain more carbohydrates, and they should probably be limited to one. If nutrition labels are available, check to see what the lowest-carbohydrate beer options are. Coolers and ciders are to be avoided due to their high sugar content.

Be kind to yourself and don’t overthink it

If you take into consideration all of the recommendations above, there is no reason to be stressed or anxious about your diet as you enter into the holidays. You are following a ketogenic diet to improve your health, right? Well, being kind to yourself is part of healthy living, and sometimes that means accepting that your diet can’t always be perfect. Also, keep in mind that you can always jump right back into the swing of things; a few days of indulging does not mean you have “failed.” There is more to health than simply what you put in your mouth, so do the best you can, be prepared, but most importantly, don’t get down on yourself if things don’t go as planned. Instead of focusing on your food options, focus on enjoying your time with loved ones over this holiday season.

As we said, the holidays are the most wonderful time of the year, and your diet shouldn’t change that for you.

General Wellness, Ketogenic

Shared by Dr. Phil McAllister @ Forward Health Guelph

Resources:

  1. McCarty MF et al. Lauric acid-rich medium-chain triglycerides can substitute for other oils in cooking applications and may have limited pathogenicity. Open Heart. 2016;3(2):e000467.

Dr. Phil Shares: Insulin Resistance Causes and Symptoms

One in three North Americans—including half of those age 60 and older— have a silent blood sugar problem known as insulin resistance. Insulin resistance increases the risk for prediabetes, type 2 diabetes and a host of other serious health problems, including heart attacks, strokes and cancer.

What is Insulin Resistance?

Insulin resistance is when cells in your muscles, body fat and liver start resisting or ignoring the signal that the hormone insulin is trying to send out—which is to grab glucose out of the bloodstream and put it into our cells. Glucose, also known as blood sugar, is the body’s main source of fuel. We get glucose from grains, fruit, vegetables, dairy products, and drinks that bring break down into carbohydrates.

How Insulin Resistance Develops

While genetics, aging and ethnicity play roles in developing insulin sensitivity, the driving forces behind insulin resistance include excess body weight, too much belly fat, a lack of exercise, smoking, and even skimping on sleep.4

As insulin resistance develops, your body fights back by producing more insulin. Over months and years, the beta cells in your pancreas that are working so hard to make insulin get worn out and can no longer keep pace with the demand for more and more insulin. Then – years after insulin resistance silently began – your blood sugar may begin to rise and you may develop prediabetes or type 2 diabetes. You may also develop non-alcoholic fatty liver disease (NAFLD), a growing problem associated with insulin resistance that boosts your risk for liver damage and heart disease. 5

Signs and Symptoms of Insulin Resistance

Insulin resistance is usually triggered by a combination of factors linked to weight, age, genetics, being sedentary and smoking.

– A large waist. Experts say the best way to tell whether you’re at risk for insulin resistance involves a tape measure and moment of truth in front of the bathroom mirror. A waist that measures 35 inches or more for women, 40 or more for men (31.5 inches for women and 35.5 inches for men if you’re of Southeast Asian, Chinese or Japanese descent)increases the odds of insulin resistance and metabolic syndrome, which is also linked to insulin resistance.

– You have additional signs of metabolic syndrome. According to the National Institutes of Health,in addition to a large waist, if you have three or more of the following, you likely have metabolic syndrome, which creates insulin resistance.

  • High triglycerides. Levels of 150 or higher, or taking medication to treat high levels of these blood fats.
  • Low HDLs. Low-density lipoprotein levels below 50 for women and 40 for men – or taking medication to raise low high-density lipoprotein (HDL) levels.
  • High blood pressure. Readings of 130/85 mmHg or higher, or taking medication to control high blood pressure
  • High blood sugar. Levels of 100-125 mg/dl (the prediabetes range) or over 125 (diabetes).
  • High fasting blood sugar (or you’re on medicine to treat high blood sugar). Mildly high blood sugar may be an early sign of diabetes.

– You develop dark skin patches. If insulin resistance is severe, you may have visible skin changes. These include patches of darkened skin on the back of your neck or on your elbows, knees, knuckles or armpits. This discoloration is called acanthosis nigricans.8

Health Conditions Related to Insulin Resistance

An estimated 87 million American adults have prediabetes; 30-50% will go on to develop full-blown type 2 diabetes. In addition, up to 80% of people with type 2 diabetes have NAFLD.9 But those aren’t the only threats posed by insulin resistance.

Thanks to years of high insulin levels followed by an onslaught of cell-damaging high blood sugar, people with insulin resistance, prediabetes and type 2 diabetes are at high risk for cardiovascular disease. Insulin resistance doubles your risk for heart attack and stroke – and triples the odds that your heart attack or ‘brain attack’ will be deadly, according to the International Diabetes Federation.10

Meanwhile, insulin resistance and metabolic syndrome are also linked with higher risk for cancers of the bladder, breast, colon, cervix, pancreas, prostate and uterus.11, 12  The connection: High insulin levels early in insulin resistance seem to fuel the growth of tumors and to suppress the body’s ability to protect itself by killing off malignant cells. 13

How You Can Prevent or Reverse Insulin Resistance

Losing weight, getting regular exercise and not skimping on sleep can all help improve your insulin sensitivity. Don’t rely on dieting or exercise alone: in one fascinating University of New Mexico School of Medicine study, published in the International Journal of Obesity, overweight people who lost 10% of their weight through diet plus exercise saw insulin sensitivity improve by an impressive 80%. Those who lost the same amount of weight through diet alone got a 38% increase. And those who simply got more exercise, but didn’t lose much weight, saw almost no shift in their level of insulin resistance.14 

Turn in on time, too. In a study presented at the 2015 meeting of the Obesity Society, researchers found that just one night of sleep deprivation boosted insulin resistance as much as eating high-fat foods for six months.15

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Dr. Phil Shares: Healthy Aging: A Functional Medicine Approach to Sarcopenia

By 2020, more than 20% of the US population will be 65 and over.1 Healthy aging is and will continue to be an important focus in many Functional Medicine offices.

Sarcopenia, the gradual loss of muscle mass that occurs in healthy adults as they age, begins after the age of 30 and accelerates after 60. The difference between the muscle mass of a 20-year-old vs. an 80-year-old is about 30%.2

Loss of muscle contributes to reduced mobility, increased hospitalizations (fragility and falls), prolonged recovery, and mortality.Factors that contribute to earlier onset and more rapid progression of sarcopenia include lack of physical activity, inflammatory conditions, blood sugar imbalances, history of smoking, hormone imbalances, and low vitamin D status.4 Addressing these risk factors is part of an individualized, preventative approach.

Therapeutic considerations that may slow this sarcopenic process down and improve overall quality of life (QOL) in an otherwise healthy, aging adult include:

Protein

Adequate, daily protein intake is essential for muscle health and possibly even more important in the aging population. Based on the evidence, the ideal protein intake for a healthy, older adult is 1.0-1.2g protein/kg body weight/day, while higher intake levels may be required in patients with acute or chronic disease.5

Achieving optimal protein intake may generally be more difficult for elderly patients at high risk for sarcopenia. Based on the results of a 2011 analysis of health and aging trends, nearly 1/2 of all US adults over age 65 have difficulty or receive help with daily activities.6 Protein powders with added BCAAs are a convenient way to support patients in meeting their protein requirements and obtain critical nutrients to help address sarcopenia.7-8

Adequate protein may also reduce risk of other age-associated events such as strokes9 and hip fractures.10 Furthermore, a practitioner does not have to wait until signs of sarcopenia are present before assessing protein requirements. In combination with physical activity, adequate protein throughout adult life may offer protection against early onset and progression of sarcopenia.11

Key clinical points:

  • Addressing increased dietary guidelines for protein intake is important for preventing loss of muscle mass in older adults7
  • Higher protein intake and lower fat mass might be positively associated with physical performance in elderly women12
  • Practitioners may help delay onset and progression of sarcopenia by assessing protein intake prior to presence of clinical signs and symptoms11

Marine omega-3 fats

The diverse, significant health benefits of omega-3 polyunsaturated fatty acids (PUFAs), namely, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are well documented. Specific to the aging population, research points to benefits in cognitive health and cardiovascular markers, as well as physical function.13

Despite the evidence, dietary intake of omega-3 fatty acids is consistently insufficient in North America, with over 90% of the population consuming <500 mg/day of EPA and DHA.14 This is a far cry from the therapeutic intake (for muscle mass and function) suggested in clinical trials of 2g-4g/day.15 Nutritional guidance around omega-3 intake provides a therapeutic opportunity for clinicians to support their aging patients.

Key clinical points

  • Supplementation with fish oil helps address the EPA+DHA nutrient gap from one’s diet14 and may help slow the decline in muscle mass and function in older adults.16
  • Increased omega-3 intake stimulates muscle protein synthesis and may be useful in prevention and treatment of sarcopenia15
  • Improvement in grip strength and muscle tone are positive benefits that may be achieved with fish oil supplementation16

Vitamin D

Vitamin D deficiency is a common occurrence in the elderly population, and its relationship to bone health is well-established. Furthermore, normal vitamin D status has also been positively correlated with functional outcomes in the elderly.18 Optimizing vitamin D status may prove to be an essential component of a protocol addressing age-related frailty and sarcopenia, especially when combined with physical activity and a protein-rich diet.17

Key clinical points

  • Treating vitamin D insufficiency and deficiency may lead to improved muscle performance, reduced risk of falls, decreased bone loss, and reduced fracture incidence18
  • Meta-analysis data indicates that serum 25-hydroxyvitamin D levels are significantly and directly associated with the risk of frailty19

Exercise

Regular exercise is important in the prevention and treatment of sarcopenia. By positively influencing blood sugar levels and body composition, physical activity helps reduce many of the risk factors associated with early onset of sarcopenia. Exercise also directly supports healthy muscle mass and function.

Whether young or old, encouraging patients to live an active lifestyle is an important and healthy addition to a sarcopenia prevention and management plan. Therapeutic benefit is optimized when fitness programs include resistance and endurance exercises 3x/week.2

Key clinical points

  • Physical activity consistently mitigates frailty and improves sarcopenia and physical function in older adults20
  • Older patients who participate in resistance and endurance exercise programs may improve not only their function and independence but also their quality of life21

The implications of sarcopenia are potentially severe. Many complications may be reduced and QOL improved with a Functional nutrition approach.

References

  1. Ortman J et al. Population Estimates and Projections Current Population Reports. https://www.census.gov/library/publications/2014/demo/p25-1140.html. Accessed September 14, 2018.
  2. Frontera W et al. Aging of skeletal muscle: a 12-yr longitudinal study. J Appl Physiol. 2000;88(4):1321-1326.
  3. Prado CM et al. Implications of low muscle mass across the continuum of care: a narrative review. Ann Med. 2018:1-19.
  4. Szulc P et al. Hormonal and lifestyle determinants of appendicular skeletal muscle mass in men: the MINOS study. Am J Clin Nutr. 2004; 80(2):496-503.
  5. N. Deutz et al. Protein intake and exercise for optimal muscle function with aging: recommendations from the ESPEN Expert Group. Clin Nutr. 2014;33(6):929-936.
  6. Disability and Care Needs of Older Americans: An Analysis of the 2011 National Health and Aging Trends Study. https://aspe.hhs.gov/report/disability-and-care-needs-older-americans-analysis-2011-national-health-and-aging-trends-study
  7. Garilli B. https://www.metagenicsinstitute.com/articles/bcaa-leucine-supplementation-increases-muscle-protein-synthesis-healthy-women/. Accessed September 14, 2018.
  8. Devries MC et al. Leucine, not total protein, content of a supplement is primary determinant of muscle protein anabolic responses in healthy older women. J Nutr. 2018;148(7):1088–1095.
  9. Zhang Z et al. Quantitative analysis of dietary protein intake and stroke risk. Neurology. 2014;83(1):19-25.
  10. Kim BJ et al. The positive association of total protein intake with femoral neck strength (KHANES IV). Osteoporos Int. 2018;29(6):1397-1405.
  11. Paddon-Jones D et al. Protein and healthy aging. Am J Clin Nutr. 2015;101(6):1339S–1345S.
  12. Isanejad M et al. Dietary protein intake is associated with better physical function and muscle strength among elderly women. Br J Nutr. 2016;115(7):1281-1291.
  13. Casas-Agustench P et al. Lipids and physical function in older adults. Curr Opin Clin Nutr. 2017;20(1):16-25.
  14. Richter CK et al. Total long-chain n-3 fatty acid intake and food sources in the United States compared to recommended intakes: NHANES 2003-2008. Lipids. 2017;52(11):917-927.
  15. Smith GI et al. Fish oil–derived n−3 PUFA therapy increases muscle mass and function in healthy older adults. Am J Clin Nutr. 2015;102(1):115–122.
  16. Smith GI et al. Dietary omega-3 fatty acid supplementation increases the rate of muscle protein synthesis in older adults: a randomized controlled trial. Am J Clin Nutr. 2011;93(2):402-412.
  17. Bauer JM et al. Effects of a vitamin D and leucine-enriched whey protein nutritional supplement on measures of sarcopenia in older adults, the PROVIDE study: a randomized, double-blind, placebo-controlled trial. J Am Med Dir Assoc. 2015;16(9):740-747.
  18. Dawson-Hughes B. Serum 25-hydroxyvitamin D and functional outcomes in the elderly. Am J Clin Nutr. 2008;88(2): 537S–540S.
  19. Ju SY et al. Kim. Low 25-hydroxyvitamin D levels and the risk of frailty syndrome: a systematic review and dose-response meta-analysis. BMC Geriatr. 2018;18(1):206.
  20. Phu S et al. Exercise and sarcopenia. J Clin Densitom. 2015;18(4):488-492.
  21. Landi F et al. Exercise as a remedy for sarcopenia. Curr Opin Clin Nutr Metab Care. 2014;17(1):25-31.

By Melissa Blake, BSc, ND

Shared by Dr. Phil McAllister @ Forward Health Guelph

Dr. Phil Shares: The Impact of Ketogenic Diet on Body Composition During Resistance Training

Ketogenic protocols have become an important therapeutic option for a variety of health issues including weight management, cardiometabolic dysfunction, and epilepsy.1 The potential of the ketogenic diet (KD) to help optimize body mass has important implications for the reduction of metabolic syndrome and its related chronic disease aspects such as heart disease, fatty liver, and type 2 diabetes (T2D).

Additionally, the ketogenic dietary approach has gained widespread attention within the professional sports performance and wellness communities for its ability to enhance weight loss and optimize body composition, both critical components in accomplishing training goals for this population.2-3 However, concerns exist in the sports performance community regarding the impact of a KD, including the possibility that lowering total body mass may reduce the ability of an individual to optimize muscle hypertrophy through resistance training (RT) due to increased central fatigue and other related factors.3

To learn more about the effects of a KD in combination with RT, a randomized, controlled, parallel arm, prospective study was conducted, with results published in the Journal of International Society of Sports Nutrition.3 The study’s authors hypothesized that, “a KD with caloric surplus in combination with RT in trained men would have a positive impact in fat reduction, and it would benefit the gains in lean body mass (LBM)”.3

Healthy, athletic men (N=24) from Spain (average age: 30, weight: 76.7kg, BMI: 23.4) with at least 2 years of continuous overload training experience were randomized into 1 of 3 groups: KD, non-KD, or control group.3 The participants followed their approved diets for 8 weeks along with supervised hypertrophy training protocol 4 days/week: 2 days of upper body and 2 days of lower body workouts. The KD group was monitored weekly by measuring urinary ketones with reagent strips to ensure they achieved and remained in ketosis. Body composition was assessed using DXA.

Participants all consumed a similar number of calories, which was set for a moderate energy surplus of 39 kcal/kg/day.3 The KD group consumed 20% of calories as protein (2g/kg/day), 70% as fat (3.2g/kg/d), and <10% of their calories as carbohydrates (approximately 42g/d).3 The non-KD consumed the same 20% of calories as protein (2g/kg/day), 25% as fat, and the remaining 55% as carbohydrates.3 Both groups were encouraged to eat 3-6 meals per day, and individuals in the control group were asked to maintain their current exercise and dietary routines throughout the study.

Results:3

  • KD: ↓ fat mass (FM) and ↓ visceral adipose tissue (VAT); non-significant reduction in total body weight; non-significant increase in lean body mass (LBM)
  • Non-KD: No significant changes in FM or VAT; significant ↑ in total body weight and ↑ LBM
  • Control: No significant changes in FM, VAT, total body weight, nor LBM

The overall results indicate the KD intervention was able to achieve a positive change in body composition with a decrease in body weight (non-significant) and reduction in FM and VAT.3 LBM did not increase significantly in the KD group, and the results indicate that LBM may be enhanced through an adequate carbohydrate intake (as was provided in the non-KD and control group diet protocols of this study) while also consuming a calorie surplus with a higher protein intake to support muscle hypertrophy.3

In summary, the implementation of a KD in male athletes taking part in regular resistance training may lead to lowering of VAT and FM, both important factors for body mass optimization and reducing risk of cardiometabolic disease processes.3 However, the lack of lean body mass accrual in this study indicates that the KD  may not be an optimal strategy for building muscle mass in trained athletes when utilized alongside a resistance training program.3 Longer study duration with larger samples, both genders, and less fit individuals (e.g. overweight) would be valuable for further exploration.

Why is this Clinically Relevant?

  • KD in trained men combined with resistance training protocols may improve VAT and FM levels, both risk factors for cardiovascular disease3
  • Trained men desiring to increase LBM and increase muscle hypertrophy may need to consider a dietary approach which includes a calorie surplus with high protein content along with adequate carbohydrate intake

View the article

Citations

  1. Paoli A et al. Beyond weight loss: a review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets. Eur J Clin Nutr. 2013;67(8):789–796.
  2. McSwiney FT, Wardrop B, Hyde PN, Lafountain RA, Volek JS, Doyle L. Keto-adaptation enhances exercise performance and body composition responses to training in endurance athletes. Metabolism. 2018;81:25-34.
  3. * Vargas S, Romance R, Petro J, et al. Efficacy of ketogenic diet on body composition during resistance training in trained men: a randomized controlled trial. J Int Soc Sports Nutr. 2018;15:31.

*Note: In the Vargas S et al. 2018 article, there are discrepancies in body composition outcomes in the written Results section of the article, however, the quantitative results in Table 2 and the Abstract are correct and are summarized above.

Shared by Dr. Phil McAllister @ Forward Health Guelph

Written by Bianca Garilli, ND