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The incidence of type II diabetes has increased world wide resulting from an interaction between a genetic predisposition fueled by behavior and environmental factors. Diet and exercise are considered important components of the treatment for type II diabetes. Together they can improve insulin sensitivity and potentially reduce the need for oral medication or exogenous insulin.

The consensus on dietary interventions is to increase consumption of fruit and vegetables, decrease consumption of saturated fat, and engage in regular physical activity. These modifiable lifestyle factors are certainly not exclusive to an individual with Type II diabetes rather are appropriate for anyone just with a desire to live a healthy life (1).

Data from The Third National Health and Nutrition Related Examination Survey explored common lifestyle factors specifically those living with type II Diabetes to uncover the amount of people engaging in these basic common habits to reduce their symptoms related to Type II Diabetes. The national survey examined the self-reports of 1,480 adults ages 18+ diagnosed with type II diabetes and analyzed diet and exercise habits. Of those with type II, nearly one-half reported no regular physical activity while 38% reported insufficient levels of activity based on the CDC’s recommendations. The majority of those surveyed reported a diet that was high in saturated fat and consumed fewer than the minimum recommended servings of fruits and vegetables (1).

Perhaps this large sample population needs some supportive evidence to encourage them to take advantage of there free interventions to control their diabetes?

Tuomiletho, J et al examined the positive effect moderate lifestyle changes had on the likelihood of developing Type II Diabetes. The design of the intervention took place during a 6-year period. Subjects were recruited based on risk factors including overweight (25BMI+), impaired fasting glucose (defined as 140-100mg/dl), and age 40-65 years old (2).

A total of 523 subjects were randomly assigned to two treatment groups. The intervention group was asked to achieve a reduction in weight of 5% or more, consume less than 30% of their energy as fat, less than 10% saturated fat, increase fiber to 15gm per 1000cal, and increase consumption of whole grains vegetables, fruits, low fat dairy and low-fat meat. Subjects were supported over the course of the first year with supervised individually tailored resistance training and nutrition counseling. They then participated in an annual follow up meeting. The control group did not receive any intervention and instead maintained their normal lifestyle.

During the first year the mean weight decreased by 4.2kg +/- 5.1kg in the intervention group and at 2 year follow up weight loss remained significantly greater in the intervention group compared to the control. Fasting plasma glucose concentration decreased 2+/-12mg/deciliter for the intervention group where the control group showed an increase of 3+/-14mg/deciliter. Serum insulin concentration decreased at a faster rate in those that engaged in diet and exercise compared to those that did not. Over the experiment, the control group with no dietary or physical intervention had twice the incidence of diabetes diagnosis compared to the intervention group: the cumulative incidence of diabetes after 4 years was 11% compared to 23% in the control group. During the 1^st year trial, the risk of diabetes was reduced by 58% in those that received support with dietary and physical activity interventions (2). Maintaining a healthy weight, limiting saturated fat, and engaging in weekly physical activity are rules everyone should live by, so it comes as no surprise that adults at risk for type II diabetes show improvement just by engaging in some healthy lifestyle choices.

It seems rather obvious that eating fruits and vegetables, exercising, and limiting saturated fat are simple modifiable lifestyle habits and these studies confirm what we already know. Obviously, the purpose of this article is to equip you with the tools to aid someone with Type II diabetes and telling a client “eat your vegetables” most certainly won’t’ elicit an epiphany moment for a client; crediting you as a great oracle that saved their disease.

Is there anything more specific one can suggest for a type II diabetic outside the scope of the same recommendations the rest of us should follow?

2 interventions that show the greatest promise for beneficial affects include a

• high dietary fiber intake and
• participating in the Mediterranean diet.

The latest recommendations from the American Diabetes Association advises against diets high in saturated fats and instead encourages consumption of mono and polyunsaturated fats as well as lean protein, low fat dairy; and fruits vegetables and whole grains that are rich in dietary fiber. The recommendation for fiber intake increased from 20 to 35gm a day because of the cholesterol lowering effects of soluble fiber.

Chandalia, M et al explored the effects of increasing intake on dietary fiber on glycemic control in patients with type II diabetes. 13 patients were randomly assigned to follow two diets for 6 weeks each. One diet contained 24gm of fiber, 8 soluble; the minimum recommended by the ADA. The experimental group consumed a high fiber diets totaling 50gm daily including 25gm of soluble fiber Macronutrient content and energy content were kept consistent with the diets and no fiber supplements were used. All fiber came solely from food (3).

Biochemical analysis included total cholesterol, lipoprotein cholesterol, triglycerides, glucose, and glycosylated hemoglobin.

• The mean plasma glucose was lower by 13mg/dL for those in the high fiber diet, and daily mean urinary glucose excretion was lower as well.
• High fiber group had 10% lower plasma glucose concentrations
• Plasma insulin was 12% lower in the high fiber group.
• A1C was slightly lower (although not statistically significant) in the high fiber group.
• High fiber diet resulted in lower fasting plasma cholesterol by 6.7%,
• High fiber group had lower plasma triglyceride by 10.2%
• High fiber group had lower fasting LDL by 6.3%. (3)

This study not only displayed the feasibility of eating a high fiber diet without added supplements, but the health benefits of the soluble fiber improved glycemic control and lowered cholesterol by binding bile acids; preventing them from being recycled for use required the body to pull from the body’s existing stores.

The foods used to reach this daily fiber goal included: Cantaloupe, grapefruit, orange, papaya, raisins, lima beans, okra, sweet potato winter squash, zucchini, granola, oat brain.

In addition to additional soluble fiber, the Mediterranean diet has had significant positive effects on preventing further progression of Type II Diabetes. The traditional Mediterranean diet is characterized by high consumption of fruits, vegetables, nuts, grains, legumes, moderate consumption of fish and wine, and low consumption of red meat and full fat dairy.

A recent clinical trial showed that a Mediterranean diet had greater glycemic control and delayed the need for antidiabetic drugs in those newly diagnosed.

Adult men and women age 55-80 years having hypertension, dyslipidemia, and overweight (risk factors for type II diabetes) were asked to consume a Mediterranean style diet meeting the following criteria: 1) Abundant use of olive oil for cooking 2) Increased consumption of fruit, vegetables, legumes, nuts, and fish 3) reduce total meat consumption 4) prepare homemade sauces with tomatoes onions and garlic, and 5) avoid butter, cream, fast foods, and sweets (4).

Weight and fasting blood glucose were recorded. The primary outcome was the onset of Type II Diabetes. 418 non-diabetics participated in the study with an average follow up of 4 years.

The incidence of diabetes was reduced by over 50% in the participants who attained at least 4 of the dietary goals over the course of the study (4). And the likely hood of developing diabetes reduced with each additional goal met. A non-calorie restricted diet enriched with high fat foods of vegetable origin decreased the incidence of diabetes in individuals at high cardiovascular risk and these risk reductions occurred in the absence of significant weight changes or implementation of physical activity. The protective effects of a Mediterranean diet with high mono and poly unsaturated fats improved fasting glucose and decreased insulin resistance (4). Specific to this study, participants were given freedom to consume up to 1 liter of olive oil each week.

Beyond the most obvious interventions- fruits vegetables and exercise; we now have supportive evidence for more specified recommendations including: 1. Fiber intake of 25grams or more and 2. High consumption of mono and poly unsaturated oils.

But what specifically about fruits and vegetables, besides their fiber content, make them so beneficial specifically to the management of type II diabetes?

Two enzymes responsible for digesting starch molecules include α-amylase and α-glucosidase. Starch molecules are first broken into smaller pieces by the enzyme amylase, and those smaller carbohydrates require glucosidase to be broken into units of glucose to enter the bloodstream for energy. Some research suggests that the phenol compounds in fruits and vegetables have an inhibiting effect on these two enzymes which would delay the carbohydrates from rapidly entering the blood stream; beneficial for treatment of type II diabetes. These natural amylase and glucosidase inhibitors from fruits and vegetables could be a helpful strategy to control post prandial hyperglycemia. “The polyphenol components of berries inhibit α-glucosidase and α-amylase enzymes, resulting in reduced blood glucose levels after starch-rich meals…potential inhibitory activity of strawberries, raspberries, blueberries and black currants on α-glucosidase and α-amylase enzymes. These authors reported that blueberries and black currants had the highest α-glucosidase inhibitory activity, and strawberries and raspberries had the highest α-amylase inhibitory activity (5).” Additionally, the leaves and fruit of avocado inhibit both alpha- amylase and alpha-glucosidase activities and can aid in the prevention of blood sugar spikes (5).

Cooked beans can protect against pancreatic beta-cell damage due to an alpha amylase inhibitor that will delay or inhibit digestion of effect carbohydrate absorption (5).

Specifically, coffee may offer some benefits to type II due to the presence of a compound called chlorogenic acid. It’s possible this acid might interact with the absorption of glucose from the intestine by inhibiting sodium dependent glucose transporters; reducing glucose’s rapid transport to the blood stream (5).

• So, fruits and vegetables, yes. But more specifically: strawberries, blueberries, black currants, cooked beans and avocados. You can even tell a client a fancy answer to further your credibility as a coach citing their potential inhibitory effects on α-glucosidase and α-amylase enzymes.
• High fiber, yes. But more specifically, a minimum 25grams with a desirable goal of 50 including 25 soluble using cantaloupe, grapefruit, orange, papaya, raisins, lima beans, okra, sweet potato winter squash, zucchini, granola, oat brain.
• Reducing intake of saturated fat, yes. Or, replacing it with liberal use of mono and polyunsaturated fats through the use of Olive Oil by up to 1 liter per week.
• Lose weight? Sure. Or how about, reducing your weight by 5% to potentially improve fasting glucose by several mg/dL and reduce glycosylated hemoglobin to lower risk of type II diabetes advancement by upwards of 58%.

Those are some specifics to get behind and certainly pack more credibility to diabetes specific suggestions than “lifestyle modification” habits. SMART (Specific Measurable Attainable Reasonable and Time Bound) goals are a great tool to help people make changes.

“Increase consumption of fruits and vegetables” may sound overwhelming but “try having a ½ cup of strawberries with breakfast this morning” with the science to back it up will help make these blurry lifestyle modifications and attainable reality while fighting a disease that affects nearly 30 million people.

References

1. Nelson KM, Reiber G, Boyko EJ. Diet and Exercise Among Adults With Type 2 Diabetes: Findings from the Third National Health and Nutrition Examination Survey (NHANES III). Diabetes Care. 2002;25(10):1722-1728
2. Tuomilehto J, Lindström J, Eriksson JG, et al. Prevention of Type 2 Diabetes Mellitus by Changes in Lifestyle among Subjects with Impaired Glucose Tolerance. New England Journal of Medicine. 2001;344(18):1343-1350
3. Chandalia M, Garg A, Lutjohann D, Bergmann KV, Grundy SM, Brinkley LJ. Beneficial Effects of High Dietary Fiber Intake in Patients with Type 2 Diabetes Mellitus. New England Journal of Medicine. 2000;342(19):1392-1398
4. Salas-Salvado J, Bullo M, Babio N, et al. Reduction in the Incidence of Type 2 Diabetes With the Mediterranean Diet: Results of the PREDIMED-Reus nutrition intervention randomized trial. Diabetes Care. 2010;34(1):14-19
5. Lin D, Xiao M, Zhao J, et al. An Overview of Plant Phenolic Compounds and Their Importance in Human Nutrition and Management of Type 2 Diabetes. Molecules. 2016;21(10):1374.

You know that sad lazy feeling you get on a cloudy rainy day? All you want to do is stay in bed and binge watch Netflix, take a nap (or 2) and make something rich and delicious for dinner. Unless of course you live in Hawaii and have no idea how to relate to the rainy-day blues. Now take that feeling and amplify it by about 210 and you’ll begin to comprehend the feelings behind Seasonal Affective Disorder. It’s not characterized by a sad day here or there, rather it is a DSM-V mental health diagnosis, characterized by recurrent depressions that occur annually at the same time each year. During these depressions, patients typically complain of fatigue, over eating, weight gain and oversleeping.

What causes Seasonal Affective Disorder?

Serotonin, a mono-amine neurotransmitter, has a large role in the symptoms of depression and subsequently, seasonal affective disorder (SAD). It’s primarily stored in the enteric nervous system located in the gastrointestinal tract but also the central nervous system in the brain. Postmortem studies in normal humans have demonstrated marked seasonal fluctuation in serotonin concentration with the highest levels in autumn, and the lowest in winter (1). Similarly, levels of serotonin metabolites (5-HIAA) in cerebral fluid are the highest in summer and lowest in winter and spring (1). Tryptophan, an essential amino acid, is a precursor for the production of serotonin. Rapid depletion of tryptophan can provide insight to possible treatment for SAD as it influences plasma serotonin levels (1).

Lam et al conducted an experiment to explore the effects of rapid tryptophan depletion on depression symptoms in people diagnosed with SAD. Tryptophan circulates in the blood bound to the protein albumin. It competes with other amino acids for absorption across the blood brain barrier. The presence of a large AA mixture with out tryptophan will lower serum tryptophan in the brain by preventing it from entering the brain, making less available for the production of serotonin (2). Tryptophan levels can be rapidly depleted by up to 80% within 3-5 hours by administering an oral tryptophan free mixture containing large amounts of other amino acids (1).

12 participants we given large doses of amino acid to create a significant plasma decrease while refraining from exposure to light during the hours of 9-5pm. These participants had previously been receiving light therapy for treatment for their SAD. Results showed that 80% of participants experienced significant depressive and anxiety symptoms, as rated on the Hamilton Depression Rating Scale score, after depletion of serum tryptophan and a reverse in the antidepressant effects of their light therapy suggesting tryptophan plays a role in managing SAD (1).

How can we increase the absorption of tryptophan?

Unlike protein and neutral amino acids, Carbohydrates can play a role in enhancing serum tryptophan. Although a carbohydrate meal itself lacks tryptophan, a carbohydrate rich meal causes insulin secretion. Insulin, delivering glucose to the muscles and the brain, decreases plasma levels of large neutral amino acids that would ordinarily compete with tryptophan for transport across the blood-brain barrier thus allowing more to be absorbed. This large uptake of tryptophan by the brain, may increase serotonin production and potentially alleviate some of the symptoms of SAD (2). Resulting brain changes in serotonin provide a plausible mechanism whereby diet could affect behavior.

People who suffer from SAD, or anyone bored on a winter Saturday for that matter, typically tend to crave and eat carbohydrate rich food. Think homemade macaroni and cheese and chocolate chip cookies. Carbohydrate craving and consumption might not only be a symptom of the disorder but an attempt to treat it. One of the most popular biochemical hypotheses explores the theory that a carbohydrate rich meal stimulates the influx of tryptophan to the brain and serotonin production.

Danilenko, K.V., et al conducted a study examining this phenomenon by comparing a carbohydrate rich or protein rich diet’s influence depression in SAD. 16 SAD subjects were compared to 16 without the diagnosis. All subjects were provided a carbohydrate rich lunch and a protein rich lunch with 1 day in between, with 105 grams each, respectively. Depression scores were obtained with a series of mood questionnaires and revealed that the carbohydrate rich meal appeared to decrease tension, depression, and anger scores where as the protein rich meal had the adverse effect in many cases. The ratio of tryptophan to other large neutral amino acids increased following the carbohydrate rich meal and decreased after the protein rich meal. There were multiple significant interactions between meal and sequence that point to differences in psychological responses to meals. Carbohydrates affected the SAD patients more so than the “normal” patients, reporting an activating affect of the carbohydrates on their positive mood leading to the conclusion that “the ingestion of high carbohydrate meals may be a mechanism used by affected individual to regulate their own brain serotonin levels.” (2) That’s certainly not to suggest replacing Prozac with M&M’s, but it does provide insight into the eating habits of someone experiencing SAD; allowing you to tailor your intervention with a better understanding of their experience and behavior.

One of the common denominators of SAD lies within geographical location. People are more likely to suffer from SAD if they live far north or far south from the equator. What does geographical location have to do with SAD? Sunlight, the primary source of Vitamin D. Some epidemiological studies suggest low levels of vitamin D may contribute to depression. Vitamin D has receptors distributed in the brain areas associated with emotional processing and affective disorders and regulates serotonin syntheses through transcriptional activation of the tryptophan hydroxylase 2 gene (3). Although Vitamin D is found in mushrooms, egg yolks, and fortified milk its primary source is sunlight. Individuals in a range of climates often become Vitamin D deficient and don’t gain sufficiency for months. It’s possible seasonal changes in Vitamin D levels may account for seasonal depressive symptoms. Kerr et al examined this phenomenon by exploring the relationship between serum vitamin D levels and depressive symptoms in 185 undergraduate college age women living in the pacific north west over a 4-week period. Consistent with their hypothesis, there was a significant correlation between diminished Vitamin D levels and depressive symptoms. At each of the 5 observation points in the experiment, 34-42% of participants reported clinically significant depressive symptoms with rates of vitamin d deficiently at a consistent rate of 31%. Mean depressive symptoms were reported more in women with lower Vitamin D levels and were lowest in the fall than any other term (4). It would be great to suggest a beach vacation as a dietary intervention for SAD treatment, but a less expensive option may be Vitamin D supplements in the amount of 500-1000IU as affective (and affordable) way to ensure you’re getting enough “sunshine” during the months when the sun sets before you step out of your office door. While you’re at the pharmacy, it might be worthwhile to pick up a DHA supplement as well. Either that or grab a nice salmon filet; as seafood is the greatest source of this omega-3 fatty acid. DHA is the brains building block. This omega-3 fatty acid provides structure to neurons and is an anchor point for neurotransmitter receptors. The densities of dopamine and serotonin receptors are dependent on DHA levels and influence the hippocampus and hypothalamus; responsible for hormone production. 1-3gm a day may help assist with seasonal affective disorder (4).

Some facilities are using these dietary interventions currently as treatment for patients with SAD. Study in Europe conducted a postal and web-based survey to 100 institutions treating more than 3100 SAD patients shared their recommended treatments for SAD. The primary interventions are light therapy however 47% of the institutions treating SAD recommended dietary changes as an intervention for alleviating SAD and of all the option, 71% of patients were treated as such. Intervention included: Mediterranean diet with an emphasis on DHA, more fiber and less meat; supplementing with Vitamin D, reducing heavy evening meals, limiting alcohol, and supplementing with B12 and Iron (5).

There are those who can’t wait for winter, and then there are those who can’t wait for winter to be over. Whether you fall into either category, the winter blues are no joke. If you or anyone you work with seems to be eating a lot more macaroni and cheese than normal and losing their stamina to make it to the gym, or even to get up and brush their hair; you have some insight to what might be going on. Fortunately, there are some dietary interventions that may assist you or your clients getting through the winter season that doesn’t mandate they buy a condo in key west. A balance of healthy carbohydrate sources like fruits, vegetables, whole grains (ok fine and an occasional brownie), Vitamin D, some nice wild caught fish (or capsule form if fish isn’t your thing) and of course non-judgmental unconditional support for those days were sweatpants are the only clothes that matter.

References

1. Lam, R.W., 1996. Effects of Rapid Tryptophan Depletion in Patients With Seasonal Affective Disorder in Remission After Light Therapy. Archives of General Psychiatry 53, 41
2. Danilenko, K.V., Plisov, I.L., Hébert, M., Kräuchi, K., Wirz‐Justice, A., 2008. Influence of Timed Nutrient Diet on Depression and Light Sensitivity in Seasonal Affective Disorder. Chronobiology International 25, 51–64
3. Kerr, D.C., Zava, D.T., Piper, W.T., Saturn, S.R., Frei, B., Gombart, A.F., 2015. Associations between vitamin D levels and depressive symptoms in healthy young adult women. Psychiatry Research 227, 46–51
4. Mahan, L.K., Escott-Stump, S., Krause, M.V., 2008. Krauses food & nutrition therapy. W.B. Saunders, Philadelphia
5. Nussbaumer-Streit, B., Winkler, D., Spies, M., Kasper, S., Pjrek, E., 2017. Prevention of seasonal affective disorder in daily clinical practice: results of a survey in German-speaking countries. BMC Psychiatry 17.

Originally written for Nutritional Coaching Institute Seasonal Affective Disorder | Nutritional Coaching Institute (ncicertifications.com)

IBS. Three little letters that carry a lot of weight. More commonly known as Irritable Bowel Syndrome, it’s a common chronic functional gastrointestinal disorder that causes pain, discomfort, bloating, and altered bowel habits.

The global presence is 11.2% but the incidence of the disease is higher in western countries affecting 10-20% of the adult population and twice as likely among women.

The mechanism remains unclear but altered gastrointestinal motility, changes to gut microbiota, altered brain gut axis, low grade digestive track inflammation and psychological factors may all play a role.

There is currently no diagnostic biomarker for IBS so it is often diagnosed based of symptoms using what’s called the Rome IV criteria and ruling out celiac disease. Rome IV criteria require the presence of recurrent abdominal pain, associated with two or more of

• pain related to defecation
• change in frequency and/or form of stool
• additional symptoms such as abdominal pain, bloating, acid regurgitation, nausea, vomiting, distention, and borborygmus aka belching.

That is a lot of discomfort for nearly 20% of adults to experience on a regular basis. Or perhaps, irregular basis is more accurate.

With so many potential factors contributing to IBS, dietary triggers are reported to be central to the symptom affecting 50-84% of patients with IBS.

The most commonly reported foods that trigger these symptoms are those containing lactose (e.g. milk); fructose (e.g. honey, dates, oranges, cherries, apples, and pears); gas producing foods (e.g. beans cabbage and bran); and sweeteners (e.g. sorbitol, mannitol and xylitol). This would suggest that dietary interventions excluding these common triggers may be helpful treatment.

But what is the common thread among these foods?

Three little letters have met their six-letter match. FODMAP. No, its not a video game, or a shake supplement or trending internet meme. Its an acronym used to describe

Fermentable

Oligosaccharide

Disaccharide

Monosaccharide

And

Polyols.

But wait. You’re not a scientist and have never heard of these things before. How on earth is this supposed to help you avoid chronic stomach pain and trips to the bathroom?

Simply put, these complicated sounding terms are the highly fermentable components of carbohydrates that cause an increase of gas, bloating, and stomach discomfort. Ever have a beer? Or if you’re under 21, Kombucha? Then you may know it is fermented, giving it that bubbly taste. Fermentation is the enzymatic or bacterial extraction of energy from carbohydrates in the absence of oxygen, producing carbon dioxide as a result. Well that’s exactly what these carbohydrate components do in your stomach. And when they ferment in your gut, they increase the water content into your bowel and increase gas by feeding your colonic bacteria. Sort of like yeast feeding on sugars to make your beer both alcoholic and fizzy.

Now that you understand the concept, lets dive into a little more of where to find these culprits.

Oligosaccharides are made of small bunches of monosaccharides aka the tiny little building blocks of all carbohydrates. They include fructans (e.g. wheat, onion and garlic) as well as alpha galacto-oligosaccharides (e.g. beans and pulses). All humans lack enzymes that hydrolyze these therefore they aren’t able to be digested and absorbed. Instead they get fermented by the colon, causing gas and in those with IBS, additional symptoms.

Lactose in milk is an example of a disaccharide, or 2 monosaccharides bonded together, which requires the enzyme lactase in order to be digested. Without that enzyme, water is drawn into the colon to dilute the lactose and it’s fermented by your gut bacteria creating gas and distension.

Fructose is a monosaccharide that some people aren’t able to absorb. Glucose is another monosaccharide but helps with fructose metabolism. If fructose is present in high concentrations like in, say, fruit juice or soda, it can lead to high levels of fructose in the small intestine which increases small intestinal water and may lead to an array of gut symptoms like diarrhea. This is actually how prune juice and apple juice help when little kids are constipated.

Polyols include sorbitol (e.g. apple and pear), mannitol (e.g. mushroom and cauliflower) and xylitol (e.g. artificial sweeteners) and are passively absorbed along the small intestine. For those sensitive to foods high in Polyols there may be an increase of small intestinal water and as a result, gut discomfort.

The aim of a low FODMAP diet is to eliminate higher FODMAP items for a period of up to 4 weeks and slowly begin reintroducing them one at a time in a period of 3-day intervals of increasing amounts. For example, adding mango for 3 days to establish tolerance for fructose or bread, onions or garlic to establish tolerance for fructans.

Several meta-analysis and cohort studies have shown that between 57-72.1% of patients experience relief when participating in modified FODMAP diet planning. One study concludes, “a low FODMAP diet significantly improves general symptoms in patients with IBS compared to standard dietary recommendations with high FODMAP foods”.

Great. There is a credible solution to your chronic stomach pain: avoid high FODMAP foods but….. what are they?!! Great question. If you can’t remember how many calories were in your cereal, how could you possibly know how much fructan is in….wait what is a fructan again?

Fortunately, a group of scientists did the work to provide the answers for you.

Lactose was first studied in the 1950s, Fructose and polyols in the 1970s and eventually fructans by 1987. But a group of scientists from Monash University in Australia (named the Monash group) decided to group these culprits together using the term FODMAP in 2004 and published their research hypothesis in Alimentary Pharmacology and Therapeutics in 2005. After their hypothesis was published, an intensive program of research was launched including a comprehensive analysis to determine the amount of FODMAPs in carbohydrate containing foods to come up with a comprehensive list and rating for nearly all foods to help the public navigate exactly what to eat. That list is now publicized on both www.ibsdiets.org as well as www.monashfodmap.com

But to help you get started, here’s a brief list

Having IBS doesn’t mean you have to abstain from all high FODMAP foods. Its completely possible that Asparagus has never bothered your stomach and never will. But with a map of possibilities, playing detective with your diet may lead you to discover after a few heavy garlic pastas followed by late nights full of Tums and Alka-Seltzer, garlic may be a trigger for you. The best way to navigate this labyrinth of food choices is by listening to your gut, literally. Pay attention to symptoms, keep a list handy of possible culprits, and work with a dietician on a plan to get you feeling better.

References

1. Whelan K, Martin LD, Staudacher HM, Lomer MCE. The low FODMAP diet in the management of irritable bowel syndrome: an evidence-based review of FODMAP restriction, reintroduction and personalisation in clinical practice. Journal of Human Nutrition and Dietetics. 2018;31(2):239-255.
2. Weynants A, Goossens L, Genetello M, Looze DD, Winckel MV. The long‐term effect and adherence of a low fermentable oligosaccharides disaccharides monosaccharides and polyols (FODMAP) diet in patients with irritable bowel syndrome. Journal of Human Nutrition and Dietetics. 2019;33(2):159-169.
3. Gibson PR. History of the low FODMAP diet. Journal of Gastroenterology and Hepatology. 2017;32:5-7 https://onlinelibrary.wiley.com/doi/pdf/10.1111/jgh.13685

Our body is composed of up to 65% water, although after this hot summer, maybe more like 57%. Anyone else sweat just by sitting still this summer? Water is used by all organs of the body, serving as a transportation system for nutrients, and metabolic reactions. The ubiquitous rule we’ve all heard about how much to drink is 8 glasses a day. It’s difficult to apply one universal amount for all human bodies. I doubt Dwayne “The Rock” Johnson and Danny Devito have the same fluid requirements, so a more appropriate universal rule: 35ml/Kg is just fine. That would mean a 70kg adult would need about 2.4 Liters of water a day to be properly hydrated.

Dehydration, by definition, is a deficit in total body water with an accompanying disruption of metabolic process. Dehydration can occur in extreme temperatures, from lack of consumption of fluids, or through sweat during prolonged exercise. Exercising while dehydrated includes increased cardiovascular strain, increased heat strain, altered central nervous system function, altered metabolic function. (1)

During heat stress, like the summer of 2018, dehydration can compromise one’s athletic performance. A meta-analysis conducted by Cheuvront et al found that dehydration of 2-7% of body weight consistently decreased endurance performance. Temperatures played a role on performance as well. Dehydration of at least 2% or greater of body weight reduced exercise performance by about 40% on a hot dry climate. That’s a large margin of performance loss that could be largely recovered if proper hydration protocols are followed. Cheuvront et al found only a 20% reduction in performance output when a 2% body weight dehydration occurred in a cool climate as it allowed increases central blood volume and lowered core body temperature (1).

Ultimately, in all temperature conditions dehydration by 1-2% doesn’t appear to alter performance when under 90 min duration. This means the sweat from a typical Saturday Pilates class or after work jog won’t have a negative impact on your speed or number of sit ups, but dehydration over 2% in hot environments is when you might see a decline in performance (2).

Now we know dehydration in amounts greater than 2% of body weight, especially in extreme temperatures, can have a negative effect on performance. But how does one remedy this? Does timing and amount of water matter?

One of the largest meta-analysis of its kind found that “drinking according to the command of thirst was associated with an increase in power output compared with a rate of drinking below…and above. The probability that drinking to the dictate of thirst confers a real and meaningful practical advantage on performance under field conditions compared with drinking below and above thirst sensation is of the order of 98% and 62%, respectively” (3).

Well, it may sound obvious but: obey your thirst. Drink according to thirst cues. According to Goulet et al, repeated replenishment and satisfaction of thirst throughout exercise should preserve extracellular fluid homeostasis and maximize endurance performance (3).

If intuition is still a little too vague to give accurate advice, and concrete instructions serves you better, what exactly does drinking according to thirst cues look like? Even though Goulet’s research supports it, simply telling a client to obey their thirst may undermined your credibility and professionalism as a coach; even if that recommendation is supported with sound science!

Since 8 glasses a day doesn’t fit all, here is a more uniquely tailored method to proper hydration so your client feels individually catered to according to their needs.

First step, pre-hydration. If sufficient fluid intake in the amount of 35ml/kg have been consumed within 12 hours of the last exercise session, ideally a person should be close to appropriately hydrated. In anticipation of a prolonged exercise regimen of greater than 90 minutes, especially in hot conditions, 5-7ml/kg at least 4 hours prior to the event will suffice (4). For a 70kg individual, 350-490ml will do. For those of you not following the metric system, that would be about 1.5-2 cups of water. This will allow time for urine output to return to normal. If more fluid is still necessary, 2hrs before the event add another 3-5ml/Kg of fluid, or another cup of water for a 70kg individual. While water is essential, it’s not the only thing lost during excessive perspiration. Electrolytes like sodium and potassium are lost as well and play a vital role in maintaining core temperature and muscle contractions. Consuming beverages with about 50mEq/L of sodium will help to retain the consumed fluids, or about 1100mg for those who are a few years beyond high school chemistry atomic weight conversions (4).

For those competing in endurance activities in excessive heat, adding 2mEq/L of potassium, or 80mg, as well as 5-10% carbohydrate solution will aid to prevent dehydration and a potential decline in performance (4).

Once the activity is over, the best way to rehydrate is to replenish 100-150% of the weight lost with water which universally looks like about 1-1.5L of fluid per each kg lost. If that’s too much math, you can always just obey your thirst.

Originally written for the Nutrition Coaching Institute: https://ncicertifications.com/blog/hydration-and-supplementation-for-outdoor-sports/

References

1. Cheuvront SN, Carter R, Sawka MN. Fluid Balance and Endurance Exercise Performance. Current Sports Medicine Reports. 2003;2(4):202-208
2. Goulet ED. Dehydration and endurance performance in competitive athletes. Nutrition Reviews. 2012;70.
3. Goulet EDB. Effect of exercise-induced dehydration on time-trial exercise performance: a meta-analysis. British Journal of Sports Medicine. 2011;45(14):1149-1156
4. Shephard R. American College of Sports Medicine Position Stand: Exercise and Fluid Replacement. Yearbook of Sports Medicine. 2007;2007:254-255

Diabetes. One word with a big meaning. In order to explain what to eat if you’re a diabetic, it’s important to first establish that there are two types of Diabetes (technically three when including gestational diabetes) Type I and Type II; and they’re different from one another.

In order to distinguish the two, it’s important to understand how exactly glucose finds its way from our stomachs to our cells.

After ingestions of a large carbohydrate meal, the beta cells of the pancreas release the hormone insulin. Insulin signals receptors to travel to the brush border of the lumen allowing glucose to enter the liver, muscle, or blood cells in the form of glucose6phosphate. Here, glycolysis occurs converting the glucose into pyruvate, further oxidized into AcetylCoA where it combines with oxaloacetate for the citric acid cycle to take place extracting ATP and delivering energy to your cells. GLUT2 receptors in the liver, beta cells of the pancreas, and kidney are responsible for transporting glucose into the blood. Once in the blood, GLUT4 receptors transport glucose to the heart and muscle.

Confused? Picture it like this…. You find your neighbor’s dog loose in your back yard, immediately go outside and manage to get him on a leash to walk him home. You knock on your neighbor’s door because you don’t have a key. On the other side of the door is your neighbor (Hey John!! I found Rex loose in my yard). John grabs the leash and takes Rex inside, thanks you and shuts the door. YOU are insulin. Rex is glucose. And John, aside from an irresponsible dog owner, is the GLUT receptor waiting to let glucose (Rex) into the cell (John’s house).

So what makes Type I different from Type II?

By definition, “Type I Diabetes is an autoimmune disease. The primary defect is pancreas Beta cell destruction, usually leading to an absolute insulin deficiency resulting in hyperglycemia, polyuria, polydipsia, weight loss, dehydration, and ketoacidosis.” The rate of beta cell destruction can vary; proceeding rapidly in some, but more slowly in others. The capacity of a healthy pancreas to secrete insulin is far in excess what is needed and can be preceded by a period of months to years during which beta cells ae undergoing chronic destruction.

This type of diabetes is typically diagnosed by early to mid-childhood and accounts for 5-10% of all diabetes cases. People with Type I can must take exogenous insulin which comes in an array of types: short or rapid acting, intermediate, or long term.

Type II Diabetes is a different story. This type of Diabetes accounts for 90-95% of all diagnosed cases. Leading contributors to Type II include adiposity and long-duration obesity. Typically, 90% of Type II cases are obese but occasionally there are people diagnosed who aren’t obese.

In most cases Type II Diabetes results from a combination of insulin resistance and beta cell failure. So, what is insulin resistance? Simply put, “decreased sensitivity or responsiveness to insulin and as a result, hyperglycemia (high blood sugar) ensues.”

A cup of spinach has between 10-12gm of carbohydrate, but also up to 8gm of fiber. Not much work on your pancreas. A 20oz coke however, well that’s 65gm of pure sugar, and no fiber to slow things down. Americans certainly drink more coke than they eat spinach, so it’s like expecting a BIC lighter to do the work of a bonfire.

Remember Rex? Well imagine you find Rex in your yard again for the 4^th time today (did somebody leave the gate open?). Instead of immediately returning him home when you hear him in your yard, you finish up a few emails, wash the dishes, and finally go out and grab him. You walk him over to John’s, but he doesn’t answer right away. You stand there getting impatient because this keeps happening and after a few minutes of tapping your foot…John finally answers. “Hey man, yeah thanks. I was watching Bird Box on Netflix and it was right at the end so…..”. Rex finally finds his way home.

Rex is glucose. And frankly, him getting loose in your yard has just made you exhausted and you’re tired of dropping everything to walk him home. This is how your pancreas feels after constantly being stressed over and over after chronic exposure to excessive glucose. So as insulin, you’re over it. Rex needs to keep his butt home. So you take your time, and so does John. As a result, Rex is hanging in limbo (like glucose in the blood stream) for a while before he finds his way home.

With Type II Diabetes, the exact mechanism of action hasn’t been found yet, but it appears the over time, the chronic stress on the pancreas causes an abnormal pattern of insulin secretion and action and also decreased cellular uptake of glucose.

Insulin resistance typically is seen primarily in muscle and adipose tissue. Inside an insulin resistant muscle, insulin loses its ability to stimulate glucose uptake. In adipose tissue, it no longer prevents free fatty acid release. Within the liver and kidney, the elevated insulin levels stimulate liver triglyceride synthesis leading to higher serum triglyceride levels. As a result, the kidney responds by increasing sodium retention but decreasing uric acid clearance. Too much uric acid is a bad thing. Erosion of organs by acid is not pleasant.

A formal diagnosis for Type II Diabetes is done with several laboratory measures.

Fasting blood glucose is taken after at least 8hrs without food. For a healthy individual, a normal blood glucose panel is 70-100mg/dl. The “at risk” range is between 100-125mg/dl. There’s also another type of blood glucose test called casual plasma glucose, which just means it wasn’t fasted and an individual most likely ate prior to the test. These levels are ideally under 200mg/dl but anything higher is an indication of type II diabetes.

High levels of glucose form a chemical bond with hemoglobin called glycosylated hemoglobin or A1C. Below 5.7% is ideal for a healthy individual whereas an A1C in the range of 5.7-6.4% suggest risk for Type II.

Physical symptoms of the disease include excessive thirst, frequent urination, polyphagia (uncontrollable hunger), and weight loss. Wait…weight LOSS? Why? Well, if suddenly insulin isn’t working well and glucose remains trapped in your blood stream, your other cells need glucose and ATP somehow. Guess what doesn’t require insulin: fat metabolism. Your body starts aggressively burning ketone bodies in order to provide some form of fuel while excessive glucose remains in your blood stream, trapped. Type II Diabetes is typically diagnosed with physical symptoms combined with fasting plasma glucose of 126mg/dl or higher.

A diagnosis can lead to interventions including medication, lifestyle changes, and calorie restriction. Recommendations for Type II Diabetics are to maintain normal blood glucose, optimal serum lipid levels, and healthy blood pressure. Some medical treatment for lowering glucose include Glucotrol which promote insulin secretion, and Glucophage (metformin) to enhance insulin action.

With long-term obesity as one of the leading contributors to Type II Diabetes, diet and exercise seem like obvious interventions to alleviate the severity of the disease. As a health enthusiast and coach, arming yourselves with efficacious dietary strategies to help Type II Diabetic clients; which is exactly what part II in this series will offer. Stay tuned.

Originally written for the Nutrition Coaching Institute; ncicertifications.com

References

1. Mahan LK, Escott-Stump S. Krauses Food & Nutrition Therapy. St. Louis, MO: Saunders/Elsevier; 2008
2. Gropper SAS, Smith JL, Carr TP. Advanced Nutrition and Human Metabolism. Boston, MA: Cengage Learning; 2018

Protein plays a large role in our body by building new muscle tissue, influencing neurotransmitters, upholding the structure and integrity of our cells as well as influencing energy metabolism and immune function.

The protein requirements for adults begin at 0.8gm/kg but the demands for an athlete are higher than those who are sedentary. Amounts safely researched vary from 1.2gm/kg-3gm/kg with higher amounts favoring weightlifters and body builders. Muscle accounts for about 40% of the protein within the human body. The more muscle, the more protein needed. Makes sense.

Protein is composed of smaller building blocks called Amino Acids (AA) of which there are 20. Nine of these AA are considered essential, meaning we must get them from food sources like meat, dairy, nuts, seeds, and legumes.

They are:

Tryptophan, Valine, Threonine, Isoleucine, Leucine, Lycine, Phenylalanine, Methionine, Histadine.

Our body uses those 9 EAA to synthesize the remaining 11. A protein is considered complete when it contains all 9 essential amino acids. Sources of protein include whole foods, protein supplements, solutions of protein hydrolysates, and free amino acids (1).

Meat and dairy are complete proteins while soy is the most complete plant-based protein; limited only by methionine. Consumption of amino acids as peptides and dipeptides result in faster absorption into the blood stream compared to the ingestion of whole proteins or single amino acids (1).

Amazon prime has a significant protein powder inventory varying from non-essential amino acids like arginine and glutamine, to complete sources like Whey or collagen, BCAA, and EAA. What’s an online shopper to do?

Arginine and glutamine are 2 popular amino acids and for good reason. AA are transmitted in muscle to their respective keto acids and are utilized for gluconeogenesis within the liver. Arginine ingestion promotes secretion of hormones that facilitate the removal of ammonia through the urea cycle (1). This is a good thing. No one wants a buildup of acidic ammonia in their body. In slow twitch muscle there’s a demand for glutamine 3x higher than fast twitch muscle suggesting a greater demand for glutamine during endurance training. Although the body makes glutamine, in times of extreme duress or exercise it is considered “conditionally essential” and additional exogenous sources are needed. Training for a marathon certainly is a condition that meets that criteria.

Of the 9 essential AA, three of them are branched; like a large oak tree with wide branches compared to a palm tree with a single stem. The three BCAA are Leucine, Isoleucine, and Valine. These three amino acids account for 15% of all amino acids in the human body. This means if a person eats 100 grams of protein a day, 15 grams will be these 3 BCAAs.

An extensive lit review by Gleeson, M. examined the efficacy of EAA/BCAA supplementation on several aspects of its role in athletic performance with positive results.

Male students aged 19-21 years engaged in 1 week of intensive exercise training including isometric exercises and elbow extensions with a 10 day recovery period and repeated this process twice. After exercise, participants were given an amino acid mixture containing all EAA (and BCAA) totaling 5.6gm or a placebo. The EAA group experienced a smaller decline in strength of elbow and isometric strength after 2 days of intense training. The AA mixture accelerated the rate of elbow extensor muscle recovery and produced higher muscle strength throughout the recovery period. Most subjects reported less delayed muscle soreness when given the AA mixture (2).

While the first study displayed positive effects of supplementing post work out with amino acids, the next study of the review examined specific amounts.

13 college athletes engaged in sustained exercise for 2-3 hours a day, 5 days a week for 6 months. During the 6-month intervention, subjects received treatments of an AA oral mix of either 2.2gm, 4.4gm, or 6.6g a day. The 2.2gm group showed no significant markers on blood measures. The 4.4gm group had significant increase in serum albumin and reduction in blood lactic acid. The 6.6gm group produced the most notable changes of reduced elevation of serum CPK (an indicator of muscle inflammation) as well an increase of hemoglobin (15.2-15.8) and hematocrit (44.9-46.8) suggesting improved oxygen handling capacity. The highest amino acid supplement had the greatest positive significant results (2).

The final study of this lit review examined the effects of administering a greater amount of AA mixture, 7.2gm daily, to 23 elite rugby players for three months during a course of intense physical training. The athletes maintained a regular training schedule, and none had previously taken AA supplementation prior to the study. Blood was collected at the end of the 3-month intervention and revealed an increase in hematocrit, hemoglobin, and iron aligning with the results of the previous study; suggesting an increased oxygen handling capacity. This increase in red blood cell production suggests the potential for AA supplementation in higher amounts potentially enhancing the capacity of the blood to carry oxygen to cells and reducing lactic acid in the blood which can improve recovery.

Overall the results of the studies in this lit review consistently displayed supportive evidence that AA supplementation had positive effects on muscle integrity, recovery, and possible enhancement of oxygen carrying capacity of blood cells improving performance.

The research suggests that Amino Acid supplementation, and more specifically Essential Amino Acid supplementation have a positive influence on performance and recovery. Is there anything that could make this better? Cake is better with a glass of milk, burgers are better with melted cheese, and protein is better with carbs. The co-ingestion of protein with carbohydrates stimulates muscle synthesis and optimizes whole body protein balance when compared with intake of protein or carbohydrate alone (1).

The primary goal of traditional post work out nutrient timing is to replenish lost glycogen stores. Replenishing glycogen stores with a rapidly absorbed form of carbohydrates (such as highly branched cyclic dextrin) when consumed immediately post exercise can replenish the rate of glycogen re-synthesis by as much as 50% when compared to ingesting carbohydrates 2 hours after exercise. Adding protein to a post work out carbohydrate meal can further enhance glycogen re-synthesis. The presence of insulin after carbohydrate ingestion helps transport amino acids to be delivered to muscle cells for repair.

Muscle protein breakdown is slightly elevated immediately post exercise and then rises shortly thereafter. As the above studies show, supplementing with AA and BCAA help improve muscle recovery. Consuming a protein/carbohydrate combination supplement within this immediate window post exercise not only replenishes glycogen stores but the presence of insulin assists with transporting AA to muscle cells, simultaneously preventing degradation through proteolysis and enhancing the effect of synthesizing new muscle tissue. A study by Levenhagen et al found that consuming an oral supplement of 10P/8C/3F immediately following exercise showed a threefold increase of protein synthesis in legs compared to just 12% three hours post work out (3).

Esmarck et al’s research displayed evidence that consuming protein immediately after training enhanced muscular growth compared to delayed protein intake. Additional studies included in this extensive lit review found that a protein/carb combination suggest a post exercise window and “delaying post work out nutrient intake may impede muscular gains”. Increase in lean body mass, positive muscular adaptations, increased muscle synthesis with the greatest affects seen in those already in shape. Makes sense why the tank top guy takes his post work out drink so seriously, while the Zumba crew bring their water and dance moves.

In practical application, “High quality protein dosed at 0.4-0.5gm/kg of LBM at both pre and post exercise is a simple, relatively fail safe general guideline that reflect the current evidence showing a maximal acute anabolic effect of 20-40gm…Pre and post exercise meals should not be separated by more than approximately 3-4hrs given a typical resistance training bout lasting 45-90minutes.” (3)

If it isn’t possible to bring a chicken breast and side of rice to the gym, a protein shake with some carbs will do just fine. With an online inventory enough to make your head spin, know this: any complete protein supplement powder will contain all EAA and subsequently all BCAA. As will a turkey sandwich. Now you know your options for optimizing your work outs is as easy as a click on amazon or just reaching in the fridge for some lunch meat.

originally written for nutrition coaching institute @ ncicertifications.com

References

1. Gleeson M. Interrelationship between Physical Activity and Branched-Chain Amino Acids. The Journal of Nutrition. 2005;135(6)
2. Ohtani M, Sugita M, Maruyama K. Amino Acid Mixture Improves Training Efficiency in Athletes. The Journal of Nutrition. 2006;136(2)
3. Aragon A, Schoenfeld B. Nutrient Timing Revisited. Functional Foods. 2013:65-89.

originally written for nutrition coaching institute @ ncicertifications.com