Showing posts with label diabetes. Show all posts
Showing posts with label diabetes. Show all posts

Tuesday, July 22, 2014

How Strong is Strong Enough to Stay Healthy? If the Sum of Your 1RMs On Leg & Bench Press Don't Surpass Twice Your Body Weight Your Risk of Metabolic Syndrome Doubles

Don't worry, the sum of both your bench and leg press 1-RM must be ~2.5x your body weight, not each of the dumbbells you use, when you do DB bench presses ;-)
As a SuppVersity reader and Super Human Radio listener, you are well aware of the vital importance of physical strength as a determinant not just of the length, but also and more importantly of the quality of your life.

Scientist from the Manitoba Institute of Child Health have now conducted the first study that was specifically designed identify the threshold of muscle strength or rather weakness that would be associated with an increased likelihood of developing metabolic syndrome in men. As Martin Sénéchal and his colleagues point out, this threshold could be used to identify men at risk of chronic disease, before it's to late to intervene. Find out if you are strong enough!
You can learn more about health at the SuppVersity

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Vit D, Soccer & Your Health

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Glutamine vs. Diabesity!
The scientists created receiver operating curves for muscle strength and the risk of MetS from a cross-sectional sample of 5685 young (<50 years) and 1541 older (>50 years) who enrolled in the Aerobics Center Longitudinal Study.

Table 1: Participant characteristics -- Continuous variables are presented as mean TSD, and categorical variables are presented a sn(%).
The primary outcome measure, the MetS, was defined according to the National Cholesterol Education Program Adult Treatment Panel III criteria. Upper and lower body muscle strength was treated as a composite measure of one-repetition maximum tests on bench and leg press and scaled to body weight.
"Low muscle strength was defined as the lowest age-specific 20th percentile, whereas high muscle strength was defined as composite muscle strength above the 20th percentile."(Sénéchal. 2014)
If you take a look at the baseline values in Table 1 on the right hand side of this paragraph, you will see that the older gentlemen in the study at hand were not just significantly unfitter, they were also fatter (waist circumference) and had - no wonder - a significantly higher rate of metabolic syndrome.

Against that background it's not surprising that the study found highly significant risk increases for metabolic syndrome in those subjects with low vs. moderate / high muscle strength. After adjustment  for age, smoking status, and alcohol intake young weaklings' risk of developing metabolic syndrome is 120% higher than that of stronger young men. For the older guys, things don't look much better.
How strong is strong enough? In order to avoid the significant increase in metabolic syndrome risk, young men have to leg press and bench press 2.86kg per kg of body weight. Older men (50+) must have an average lower body and upper body strength (assessed as 1-RM on supine bench press and seated leg press) of 2.46kg per kg body mass. With a 112% risk increase the weak 50+ agers are also more than twice as likely to develop metabolic strength.
Unsurprisingly, a further adjustment for cardiovascular fitness lead to a significant reduction of the associated risks from +120% and +112% to 23% and 32% respectively. In that, it is probably worth mentioning that strength appears to have a greater influence in older vs. younger men.

The significant impact of an adjustment for physical fitness, i.e. a measure that has all to do with cardio training (LISS / HIIT) and general physical activity and only very little with how much you lift on a 1-RM max effort should yet remind you that brute strength alone is not going to save you (fat) ass if you are one of the 21.8% of people who (dis)qualified as being inactive in their leisure time.
"Trying to Build Strength? Periodized Training Yields 30% / 34% / 77% Increases in Bench Press, Squat and Deadlift Performance" | read more
Bottom line: While we have long known that muscular weakness is a correlate of increased mortality and reduced quality of life in the elderly, the study at hand is the first to provide some orientation as to how strong you have to be to avoid health problems.

In that it may be surprising that the difference between young and old men is significantly lower than you'd expect: 14% or 0.4kg per kg body weight that's not exactly much and a value that tells us that the 65-year-old 95kg father of a 35-year-old 90kg son has to bench and leg press only ~10% less than his son (233.7 kg vs. 257.4 kg | for bench + leg press).

...What? Yes, I am pissed, too, but I hope that the scientists will soon come up with a similar study in women. I mean, we all know that muscle strength is nothing only men benefit from, right?
Reference:
  • Sénéchal, Martin, et al. "Cut-Points of Muscle Strength Associated with Metabolic Syndrome in Men." Medicine & Science in Sports & Exercise (2014).

Thursday, July 17, 2014

Surprisingly Pronounced Benefits From Glutamine Supplementation in Type II Diabetics - Human Study Shows: 3x30g/day Markedly Improved Cardiovascular Risk Factors & Body Comp in 6 Weeks

Can glutamine keep the T2D-related weight gain in check? Yes it can!
Like so many supplements, glutamine has once been all the rage and on everybody's "Must Have Supplement List" and now... well, the latest evidence from controlled human trials with athletes appears to confirm what most people believe: It's useless. Useless, unless you have increased glutamine requirements your regular diet cannot cover; and exactly this is what probably made the difference in a recent study from the Tehran University of Medical Sciences in the course of which sixty-six type 2 diabetic subjects who were 18-65 years old, were randomized to receive glutamine (30g/d) or placebo three times a day, in a double-blinded, placebo-controlled trial during 6-week treatment period.
I suppose 3x30g whole protein would have worked even better SuppVersity

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Protein requ. of athletes

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5x More Than FDA Allows
Now that's plenty of glutamine, you're right and in fact, aside from an increased baseline requirement, the mere amount of glutamine (other studies use 10-30g once, not thrice per day) is an alterative explanation for the indisputably surprising effects the provision of this conditionally essential amino acids had on the overweight, but not obese subjects.
Figure 1: Rel. changes in body composition in response to 6 weeks on 3x30g/day glutamine (Mansour. 2014)
If you take a look at the data in Figure 1 you will see that significant difference were observed for body fat mass (P=0.01), percentage of body fat (P=0.008), and the waist circumference (not shown; P<0.001) between the groups. Unfortunately, this does not mean that the subjects in the glutamine group lost weight. What it does mean, though, is that the provision of plenty of extra glutamine stopped the continuous fat gain and muscle loss that's so characteristic of type II diabetes. Moreover, the "enhancement in body fat free mass was mainly attributed to [the] trunk (P= 0.03)". In other words, the fat loss occurred right, where you want to have it if you are suffering from metabolic syndrome and intend no to end up under the ground before your time.

As it was to be expected, the reduction in trunk fat went hand in hand with a downward trend in systolic, but not diastolic blood pressure (P= 0.005), fasting blood glucose (mmol/L) concentration (P=0.04) and mean HbA1c was significantly different between the groups at week 6 (P=0.04).
The benefits were not brought about a reduction in energy intake!
Bottom line: In view of the fact that the subjects were as lazy as before and against the background that both, the glutamine and the placebo group (voluntarily) consumed less food than they were used to over the course of the six-week study period, the results Mansour et al. present in their soon-to-be-published paper in the peer-reviewed scientific journal Nutrition are more intriguing that the absence of actual weight loss may suggest. So intriguing, in fact that you got to ask yourselves why it's always the Iranians that discover / confirm those powerful effects of non-prescription, non-patentable agents like glutamine...  well, I guess, I'll leave it up to you to come up with a political correct answer to this question ;-)

What I can tell you right away, though, is that I am convinced that 3x30g of whey protein would have yielded even more intriguing results - and if you asked me: If you follow the 30g+ of protein per meal advice I have repeatedly given here at the SuppVersity you are almost certainly not going to be as glutamine deficient as the subjects in the study at hand.
Reference:
  • Mansour, Asieh, et al. "Effect of glutamine supplementation on cardiovascular risk factors in patients with type 2 diabetes." Nutrition (2014).

Thursday, May 15, 2014

Many Small Meals Suck! Especially For Diabetics. Human Study Shows 6 Small Meals Mess W/ Blood Sugar Control, Make You Hungry and Decrease The Metabolic Rate

No, no and no! Don't be stupid! Eat to satiety and fast or stay fat forever! Frequent meals will hamper not improve dietary T2DM treatment.
If you want my honest opinion, the only thing that's surprising about the following line you are about to read in all major science news outlets, today, is that it has taken scientists years to understand that "two large meals (breakfast and lunch) better than 6 small meals with same calories for controlling weight and blood sugar in people with type 2 diabetes." This is a quote from the press release that was published along with a recent paper in the scientific journal Diabetologia (the journal of the European Association for the Study of Diabetes) which "suggests that two large meals (breakfast and lunch), rather than six small meals with the same total calories, are better for controlling weight and blood sugar in people with type 2 diabetes."
You can learn more about meal frequency at the SuppVersity

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Breakfast Keeps You Lean?!

Frequent Protein Consumption

Myth: Few Meals More Bodyfat

8 Meals = Stable, But High Insulin

Int. Fasting & Exercise
The corresponding experiment was conducted by Dr Hana Kahleová from the Diabetes Centre at the Institute for Clinical and Experimental Medicine in Prague. The study assessed 54 patients (29 men, 25 women) treated with oral diabetes drugs, aged 30–70 years, BMI 27–50 kg/m2 and HbA1c of 6–11.8% (42–105 mmol/mol). They were asked to follow one of two regimens of a restricted calorie diet, each containing 500 calories less than the recommended daily amount; in one programme the meals were six small meals (A6) and the other 2 large meals, breakfast and lunch (B2).

The study was designed as a "cross over", this means all 54 participants were tested on the two and the six meal plans for 12 weeks each. Needless to say that the diet in both regimens had the same macronutrient and calorie content - otherwise, a comparison of the measured liver fat content, insulin sensitivity and pancreatic beta cell function (the cells that produce insulin) would obviously have been useless.
Figure 1: Changes in anthropometric and laboratory variables. Data are shown as changes from baseline in response to the regimen of six (A6) and two meals (B2) a day (Kahleova. 2014).
Apropos comparison, even a rocket scientist could easily tell that the data in Figure 1 speaks in favor of the two-, not the still heavily propagated "eat frequent small meals"-six-meal strategy.
If you train in the PM skip breakfast and consume launch and dinner, only! The "breakfast is the most important meal of the day"-myth is about as flawed as the "eat frequently to get / stay lean" myth (learn more). Forget it and eat according to your schedule. If you train in the morning, or at noon, skip dinner. If you train in the afternoon, skip breakfast - or, put simply: Make sure to have a meal after every workout.
In spite of the fact that the researchers found that the body weight decreased in both regimens, there was a highly significant advantage for the two-meal (B2; -3.7kg) regimen over the six-meal (A6; -2.3kg) regimen. Similarly, liver fat content (B2 -0.04% vs. A6 -0.03%), fasting plasma glucose and the pro-insulinogenic C-peptide levels decreased in both regimens - yet obviously more for the two-meal strategy.

Eating more frequent makes you hungry and will shut down your metabolism

No, that's not a typo. In total contrast to what common stupidity... ah, I mean wisdom still says, eating more frequently will not decrease your hunger, and avoid the metabolic shut-down you'll experience on every energy restricted diet, sooner or later - on the contrary!

Figure 2: The difference may not reach statistical significance, but it should be pronounced enough to lie all myths about the "metabolically activating effects of frequent meals" at rest - wtf, look at the data: Never eating to satiety is the starvation signal - and not fasting for a couple of hours per day (Kahleova. 2014).
What eating frequent small meals really does do the average lifestyle diabetic is:
  • leave him hungry even right after meals
  • elevate plasma glucagon ("hunger"-hormone) and thus increase the conversion of glycogen back to glucose
  • have his thoughts revolve around food 24/7
Similar effects with less detrimental health effects have been reported for healthy individuals as well. So that I would suggest to extend the authors' conclusion that "[t]hese results suggest that, for type 2 diabetic patients on a calorie-restricted diet, eating larger breakfasts and lunches may be more beneficial than six smaller meals during the day," (from the press release) from the average lifestyle diabetic to everyone w/ a couple of extra pounds who is trying to shed weight... The very lean athlete, on the other hand, has so little body fat to draw on and may in fact be better off with more frequent meals.
Bottom Line: This is not the first study that's questioning the general suggestion to eat more frequently to ward off and battle diabesity and I can guarantee it's neither going to be the last one.

Needless to say, snacking is a no-go as well, right? Read for yourself!
What I can guarantee, as well, though, is that it's not going to change the textbook- instead of evidence-based approach most doctors and dietitians are following. For these findings to finally make it into the day-to-day business of those people who are "dealing" with, but obviously not healing type II diabetics, it will take at least one generation of doctors and dietitians and two generations of their patients who may be paying for the delays with their lives. Lives that could have been saved if doctors and dietitians gave better advise and the patients had the guts to follow it.

Addendum: In view of warranted questions about contradictions to previous articles, I would like to point out that we are talking about a weight loss scenario with restricted energy intake, here. Not! An ad libitum diet, where eating "as often as you like", even if that may be eight times per day will help those of you who have not already ruined their "hunger gauge" (I am talking about "HUNGER" as in "NOT APPETITE") to stay lean / make lean gains. For someone whose primary goal is weight loss, I have always pointed to "intermittent fasting" (=low meal frequency) as a very feasible way to cut calories and lose weight - it does not work for everyone, though.
References:
  • Kahleova, et al. "Eating two larger meals a day (breakfast and lunch) is more effective than six smaller meals in a reduced-energy regimen for patients with type 2 diabetes: a randomised crossover study." Diabetologia (2014). Ahead of print.

Sunday, April 27, 2014

The Vitamins E & Glucose Control | Part X of the "There is More To Glucose Control Than Low Carb" | Plus: Alpha-, Gamma-, Delta-Vitamins E, Where Can You Find Them?

All nuts are good tocopherol (T) sources, but α- T is predominantly found in peanuts, almonds and sunflower seeds, while γ-T is the major vitamin E in walnuts, pecans and pistachios.
Over the past week I've been questioning the potency of various supplement superstars with respect to their ability to improve your, my or any one else's glucose metabolism. We've dealt with protein, peptides, fats, vitamin D, calcium, a whole host of B-vitamins and even the underrated vitamin A (go back and review all of them).

Today I am going to take a look at a "fallen star", vitamin E, once thought of as a panacea and universal protector of your cells, it has, at the latest with publication of the disappointing, if not shocking results of the SELECT trial in 2013 and the mass-media reverberations about increased prostate cancer risk, become the centerpiece (literally) of every anti-vitamin supplement rant.
You can learn more about this topic at the SuppVersity

Proteins, Peptides & Blood Glucose

SFA, MUFA, PUFA & Blood Glucose

Vitamin D & Diabetes

Glucose Manager Calcium?

Flush & No-Flush Niacin & Diabesity

Vitamin C & Glucose Control
Table 1: Tocopherol / -trienol compo-sition of select oils (Juang. 2014); mind the association of PUFA + γ- and MUFA + α-tocopherol.
You will probably remember that I have criticized the design and interpretation of the results of the often- and in my eyes over-cited SELECT trial on several occasions. And even if there was a +17% increase in cancer risk in young men who are stupid enough to take 400 IU of all rac-α-tocopheryl acetate, everyday (Klein. 2011), this does not necessarily exclude that the same effects occur if the vitamin E comes from a natural source and contains the whole vitamin E alphabet from alpha- over gamma to delta-tocopherol.

Not in spite of, but rather because of the existing evidence that vitamin E could cause prostate cancer and, when it's consumed with vitamin C, inhibit the beneficial adaptation processes that are triggered by the "eu-stressor" (=good stress) exercise, it is yet even more important that we take a closer look at the actual negative effects vitamin E supplements exert on your ability to control your blood sugar levels.

Vitamin E  ➫ insulin resistance ➫ cancer?

I mean, think about it: What is the best growth environment for cancer? Right, sugar coated cells - a study by Stattin et al. (2007) has after all been able to show that to an the risk of developing any form of cancer increases almost linearly from the bottom to the top quartiles of fasting and postprandial glucose levels.
Figure 1: Risk increase for various cancer if fasted [F] and post-glucose load [P] blood glucose levels are in the fourth vs. first quartile; the hazard ratios were calculated based on data from the 33,293 femal and 31,304 male subjects of the Västerbotten Intervention Project of northern Sweden (Stattin. 2007)
If we assume that vitamin E does inhibit the anti-diabetic adaptations to exercise (in conjunction with vitamin C, it does just that; cf. Ristow. 2009), it would increase the risk of having extreme blood sugar excursions, of which the data in Figure 1 reveals that they, in turn, could be the reason vitamin E was found to be associated with an increased cancer risk.
Prostate cancer and high glucose levels? Unlike other forms of cancer, prostate cancer does not appear to flourish in high glucose environments. At least that's what the epidemiological evidence suggests. Evidence which may be flawed by the existence of a genetic variant with opposite effects on risk of type 2 diabetes and prostate cancer (Gudmundsson. 2007), which could partly explain the null association between glucose and prostate cancer in our study as well as the consistently reported reduced risk of prostate cancer in men with type 2 diabetes (Kasper. 2006).
The question we have to answer in today's installment of the "There is More to Glucose Control Than Low Carb", would thus be: Does vitamin E a protective, a detrimental, or no influence on the development of insulin and type II diabetes ... and the answer is: As usually, complicated.

First things first - What actually is vitamin E?

I have already hinted at the fact that "vitamin E" is a generic term that is usually falsely applied to alpha-tocopherol, only. When we are talking about vitamin E, we do yet have to look at the whole spectrum of vitamins E, which include the three tocopherols, as well as their rare tocotrienol buddies.

Tocopherols - α-, γ, and δ- and relates substancesTocotrienols - α-, γ, and δ- and related substances
They are a class of chemical compounds many of which have vitamin E activity. This series of organic compounds consists of various methylated phenols. Because the vitamin activity was first identified in 1936 from a dietary fertility factor in rats, it was given the name "tocopherol" from the Greek words "τόκος" [birth], and "φέρειν", [to bear or carry] meaning in sum "to carry a pregnancy," with the ending "-ol" signifying its status as a chemical alcohol.
α-Tocopherol is the main source found in supplements and in the European diet, where the main dietary sources are olive and sunflower oils, while γ-tocopherol is the most common form in the American diet due to a higher intake of soybean and corn oil.
There is no RDA or other recommendation for the intake of the three most common tocopherols, i.e. α-, γ, and δ- tocopherol. The currently recommended intake for "vitamin E" is thus based on the concept of alpha-tocopherol equivalents. A very sketchy idea that's probably flawed due to significant differences in the metabolism and uptake of the various tocopherols between rodents and humans.
In view of the fact that dietary vitamin E provides - assuming you don't follow the standard American diet - a balanced mix of tocopherols, you don't really have to care about the accuracy of the conversion factors.
Tocotrienols are members of the vitamin E family. An essential nutrient for the body. The slight difference between tocotrienols and tocopherols lies in the unsaturated side chain having three double bonds in its farnesyl isoprenoid tail.
Tocotrienols are natural compounds found in select vegetable oils, including rice bran oil and palm oil, wheat germ, barley, saw palmetto, anatto, and certain other types of seeds, nuts, grains, and the oils derived from them. This variant of vitamin E typically only occurs at very low levels in nature.
At the moment we still know too little about this form of vitamin E to be able to tell how much of them you actually need. It is in fact not even sure that they are necessary at all.
Contemporary evidence does yet appear to suggest important functional differences between tocopherols- and -trienols that have the latter appear as the more potent cousins of the good old tocopherols. Furthermore, emerging evidence suggest that some long-chain vitamin E metabolites have even stronger anti-inflammatory effects than their vitamin precursors.
Unless you plan to live on artificial foods, alone, the rare tocotrienols will yet never fully replace the omnipresent tocopherols.
Table 2:Brief overview of some of the basic fact about the two main forms of vitamin E (partly based on the Wikipdia entries and on information from a soon-to-be-published review by Jiang)
This is unfortunately, where things get complicated. For one, 99% of the studies have been conducted with alpha-tocopherol, only. For two, the vast majority of the few studies that investigate potential effects of other "vitamins E" on glucose control use either another form of tocopherol, or tocotrienols. A study that would investigate the effects of the whole spectrum of vitamins E, let alone their interactions, on the other hand, has still to be conducted.

☇ Let's start with epidemiological evidence, today

That being said, out best and most realistic starting point is not the classic randomized controlled trial, but "epidemiological guesswork". As long as we are talking about food-borne vitamin E, we are always talking about a natural mix. A mix, which was (unfortunately) often measured in alpha-tocopherol units, but would, in the absence of supple of which studies show that the following associations (remember: epidemiology cannot prove cause-effect relationships)
  • Low vitamin E intakes (<10mg/day, i.e. 15IU) have been associated with and correspondingly low serum levels have been associated with 3.9x increased diabetes risk back in 1995, when vitamin E was still everybody's darling (Salonen. 1995). In view of the relatively low threshold level, this is yet rather a study that supports the notion that vitamin E is, just as the word "vitamin" implies, so vital for your health that you better make sure you get enough of it from your diet (the RDA is 15mg/day).
  • Table 3: The number of studies that distinguishes the different forms of vitamin E is low. A 2004 study by Montonen et al. does yet appear to confirm what I wrote before - they are all relevant and the the 34% reduced diabetes risk with a high dietary alpha-tocopherol intake is by no means meaningless.
    Significantly and borderline significantly reduced type II diabetes risks with all forms of tocopherols and tocotrienols in a cohort consisting of  2,285 men and 2,019 women 40–69 years of age who were free of diabetes at baseline when they were recruited for a 23-year follow-up in 1967–1972 (Montonen. 2004).

    What is particularly interesting is that the data in Table 3 clearly indicates that the good old, often ridiculed alpha-tocopherol does still have the most potent anti- diabetes effect of all 6 forms of vitamin E.

    Moreover, with beta-tocotrienol, the 2nd place is however occupied by a form of vitamin E you will find in very high amounts (30µg/g; cf. Nielsen. 2008) in whole wheat grain - is this the reason whole grains are associated with lower type II diabetes risk in epidemiological studies (Cho. 2013)?
  • High intakes (>20mg/day, i.e. only 30IU!) of vitamin E are associated with a ~20% reduced risk of developing type II diabetes in the participants of the Insulin Resistance Atherosclerosis Study (IRAS) that involved 895 nondiabetic adults at baseline (including 303 with impaired glucose tolerance [IGT]), 148 of whom developed type 2 diabetes according to World Health Organization (WHO) criteria during the 5-year follow-up (Mayer-Davis. 2002)
Epidemiology, dietary vitamin E and high dose supplementation: Most epidemiological studies still measure the alpha-tocopherol intake and serum levels. As long as there are no supplements involved, the results will yet still be representative of dietary vitamins E intake. It's after all more or less impossible to get only one form of vitamin E from whole foods.
That being said, "officially" the consumption of alpha-tocopherol-only supplements is save - at least in amounts of 60, 200, or 800 IU/day (55, 182, or 727 mg) all-rac-a-tocopherol/d will not produce noticeable side effects, changes in body weight, plasma total proteins, albumin, glucose, plasma lipids or the lipoprotein profile, the whole set of measures of organ health, as well as the levels of antioxidant vitamins and minerals (including the other forms of vitamin E; Uchida. 2013), glutathione peroxidase, superoxide dismutase, or total homocysteine of healthy elderly individuals (Meydani. 1998). Bendich & Machlin even state that vitamin E was safe up to doses of 3,200IU/day. Personally I do yet strongly advice against using more than 1,200IU of E per day (Bendich. 1988) - irrespective of whether it's alpha tocopherol or a tocopherol and -trienol blend.
  • Liver Enzymes the #1 Marker of Insulin Resistance | learn more
    Patients with non-alcoholic fatty liver disease consume on average only half the amount of vitamin E, their healthy peers do (Musso. 2003). As a SuppVersity reader you know about the intricate relation between NAFLD and diabetes, and are thus aware that this is another "pro" argument with respect to the consumption of high vitamin E foods. If this is your first visit to the SuppVersity check out my previous article "Liver Enzymes the #1 Marker of Insulin Resistance!? Plus: What Does the Correlation Bettwen HbA1C & ALT, AST and GPT Tell Us About Diabesity?" to learn more about the relationship between obesity, diabetes and non-alcoholic fatty liver disease.
On the other hand of the "foods vs. supplement divide" things are less black or white, though. While the previously cited epidemiological evidence clearly suggests that food-borne vitamin E will protect you against diabesity. On the "supplement side of things", we have both extremely promising positive experimental evidence:
  • 42% increased glucose disposal in elderly study participants in response to mediated stimulation after 4 months on a 900 mg d-alpha-tocopherol, i.e. 1350IU (!) of supplemental vitamin E per day. The fact that Paolisso et al. also observed that the "net changes in plasma vitamin E concentrations correlated with net changes in insulin-stimulated whole-body glucose disposal (r = 0.60 P < 0.003)" makes their results even more amazing (Poalisso. 1994)
  • Low vitamin E intakes early in pregnancy have been found to set women up to insulin resistance and hyperglycemia later in pregnancy by Ley et al. who write in their recent paper in the European Journal of Clinical Nutrition that (Ley. 2013) even after adjustment for serum adiponectin among women consuming daily, higher dietary vitamin E intakes were associated with lower fasting glucose, lower HOMA insulin resistance (long term measure of blood glucose), and higher Matsuda insulin sensitivity index (standard measure to quantify insulin sensitivity) among women who consumed a faily multivitamin supplement with "adequate", albeit probably synthetic vitamin E (dl-alpha-tocopherol).
The specificity principle: I am not sure if you remember the "Three Simple Rules of Reasonable Supplementation" (re-read them), but if you do, you will remember that specificity is one of the most important principles to follow, if you want to make the most of your supplement regimen. In the case of alpha-tocopherol this may mean that benefits will be seen in people with high baseline inflammation, while people without chronic inflammation, will see no, or even experience negative effects from (high) dose vitamin E supplements.
  • Modest vitamin E supplementation  (100 IU/day) can significantly lower blood glycated hemoglobin and TG levels and does not have any effect on red cell indices in Type I diabetic patients (Jain. 1996). In view of the inflammatory underpinnings of type I diabetes, this study is yet not exactly representative of the benefits a healthy individual may derive from the same amount of vitamin E... although, I have to admit that a 100IU supplement looks much more rational to me than one with 400-1,200IU - specifically if it's pure alpha-tocopherol.
  • High dose (800-1200 IU/day) vitamin E supplementation improves fasting blood glucose and HbA1c levels in obese subjects - eighty overweight individuals (BMI >27 kg/m²), to be precise, who  were randomly allocated to receive either 800 IU vitamin E per day or a matching placebo for 3 months. The dose of vitamin E was increased to 1,200 IU per day for a further 3 months (Manning. 2006).
On the other hand, we have experimental evidence that refutes the previously reported beneficial effects of supplemental vitamin E on blood glucose management. Examples? Here you go:
  • And what about exercise: Aside from the previously mentioned negative effects on the adaptation triggering exercise induced eustress, there are no good reasons to avoid vitamin E supplements for athletes. In fact, my previous analyses of corresponding studies here at the SuppVersity would suggest that people with a high baseline inflammation that overrides the exercise-induced locally confined increase in inflammation, may have good reason to take up to 400 IU/day of mixed tocopherols (opt. -trienols) - specifically if their vitamin E intake from foods is low, like on a diet, for example.
    600 IU/day of vitamin E taken every other day provided no significant protection against type 2 diabetes in initially healthy women in the Women’s Health Study randomized trial (Liu. 2006). A study that appears to confirm that supplementing additional antioxidants is, just like keeping your omega-3/omega-6 ratio up (learn more), useless, unless it's part of an overall healthy life-style - and in that case, there is still the nasty question: Will it negate the beneficial effects of exercise or not?
  • In general, vitamin E supplementation does not decrease all-cause mortality or cardiovascular disease risk in type II diabetes. This is at least what a 2003 meta-analysis of studies with 81,788 concluded. As Vivekananthan et al. point out, "the lack of a salutary effect was seen consistently for various doses of vitamins in diverse populations" (Vivekananthan. 2003)
Of particular interest for us is the conclusion Vivekananthan et al. draw based on the results of their meta-analysis: If their results "do not support the routine use of vitamin E" this does after all mean that we don't have to argue about whether or not antioxidants negate the beneficial effects of exercise or whether "high-dosage vitamin E supplementation may increase all-cause mortality" as Miller et al. (2005) suggest in a 2005 meta-analysis in the Annals of Internal Medicine - Why? Well, why would we care about negative side effects, if it's not worth using them, anyways!?
α-tocopherol: Veggies (spinach, broccoli, tomato paste, everything that's orange); eggs; almonds, peanuts, sunflower seeds; olive & almond oil.
γ-tocopherol: tomotoes, tuna; eggs; walnuts, pecans, pistachios and sesame seeds, pine nuts; dark chocolate or baking chocolate; seeds & grains, flax, peas, lentils; corn, soybean & canola oil, margarines, all sorts of shortenings and fried foods that are prepared with high γ-tocopherol oils
δ-tocopherol: peppers, onions, tomato seeds; raspberries, black- berries; tuna, mol- lusks, eggs; edamame; orega- no; rice germ oil, soy- bean oil, all sorts of shor- tenings and fried foods that are prepared with high δ-tocopherol oils
Don't supplement, eat your vitamins E: Not using vitamin E supplements (for glucose management) does yet also imply that you have to get your vitamins E from dietary sources. In view of an RDA of only 15mg and evidence that 100mg of vitamin E is already plenty, this does not appear to be difficult, but if you look at the total amount of vitamin E in the average American diet, you will be surprised that (a) gamma- and not α-tocopherol is the major form of vitamin E in the vegetable oil laden US diets (~60-70 % γ- vs. 20-25% α-tocopherol; cf. McLaughlin. 1979) and that (b) more than 80% of the Americans who don't supplement and still 45% of those who take supplements are effectively vitamin E deficient (McBurney. 2014).

There is little doubt that McBurney's observations are partly related to the increase vitamin E requirements of a lifestyle that is characterized by junk-food diet, sedentarism and chronic inflammation. They are yet also a result of a lack of foods that are naturally high in vitamin E, and supply you with both, the full spectrum of tocopherols and -trienols and the necessary co-factors to make the most of your dietary vitamins E intake - in short, it's a lack of the foods in the list on the right. Foods of which I assume that I will find the healthy ones (in italics) on your plate regularly, right?

What? Oh, yes. Well, the tocotrienols are in fact a problem. With the exception of red palm oil (50-75mg/100g) you will find only trace amounts (all values in mg/100g) of them in various fats/oils like rice wheat germ oil (18.9), coconut oil (2.1), and cacao butter (0.2) and grains like barley (91) and oats (21).
Reference: 
  • Bendich, A., and L. J. Machlin. "Safety of oral intake of vitamin E." The American journal of clinical nutrition 48.3 (1988): 612-619.
  • Cho, Susan S., et al. "Consumption of cereal fiber, mixtures of whole grains and bran, and whole grains and risk reduction in type 2 diabetes, obesity, and cardiovascular disease." The American journal of clinical nutrition 98.2 (2013): 594-619.
  • Gudmundsson, Julius, et al. "Two variants on chromosome 17 confer prostate cancer risk, and the one in TCF2 protects against type 2 diabetes." Nature genetics 39.8 (2007): 977-983. 
  • Jain, Sushil K., et al. "Effect of modest vitamin E supplementation on blood glycated hemoglobin and triglyceride levels and red cell indices in type I diabetic patients." Journal of the American College of Nutrition 15.5 (1996): 458-461. 
  • Jiang, Qing, et al. "γ-Tocopherol, the major form of vitamin E in the US diet, deserves more attention." The American journal of clinical nutrition 74.6 (2001): 714-722.
  • Jiang, Qing. "Natural forms of vitamin E: Metabolism, antioxidant and anti-inflammatory activities and the role in disease prevention and therapy." Free Radical Biology and Medicine (2014).
  • Kasper, Jocelyn S., and Edward Giovannucci. "A meta-analysis of diabetes mellitus and the risk of prostate cancer." Cancer Epidemiology Biomarkers & Prevention 15.11 (2006): 2056-2062.
  • Klein, Eric A., et al. "Vitamin E and the risk of prostate cancer: the Selenium and Vitamin E Cancer Prevention Trial (SELECT)." Jama 306.14 (2011): 1549-1556.
  • Ley, S. H., et al. "Lower dietary vitamin E intake during the second trimester is associated with insulin resistance and hyperglycemia later in pregnancy." European journal of clinical nutrition (2013).
  • Liu, Simin, et al. "Vitamin E and risk of type 2 diabetes in the women’s health study randomized controlled trial." Diabetes 55.10 (2006): 2856-2862. 
  • McBurney, Michael, et al. "Vitamin E status of the US adult population by use of dietary supplements (1041.7)." The FASEB Journal 28.1 Supplement (2014): 1041-7.
  • Manning, Patrick J., et al. "Effect of high-dose vitamin E on insulin resistance and associated parameters in overweight subjects." Diabetes Care 27.9 (2004): 2166-2171.
  • Mayer-Davis, Elizabeth J., et al. "Plasma and Dietary Vitamin E in Relation to Incidence of Type 2 Diabetes The Insulin Resistance and Atherosclerosis Study (IRAS)." Diabetes Care 25.12 (2002): 2172-2177. 
  • McLaughlin, P. J., and John L. Weihrauch. "Vitamin E content of foods." Journal of the American Dietetic Association 75.6 (1979): 647-665.
  • Meydani, Simin Nikbin, et al. "Assessment of the safety of supplementation with different amounts of vitamin E in healthy older adults." The American journal of clinical nutrition 68.2 (1998): 311-318.
  • Miller, Edgar R., et al. "Meta-analysis: high-dosage vitamin E supplementation may increase all-cause mortality." Annals of internal medicine 142.1 (2005): 37-46.
  • Montonen, Jukka, et al. "Dietary antioxidant intake and risk of type 2 diabetes." Diabetes Care 27.2 (2004): 362-366. 
  • Nielsen, Merete Møller, and Åse Hansen. "Rapid high-performance liquid chromatography determination of tocopherols and tocotrienols in cereals." Cereal chemistry 85.2 (2008): 248-251.
  • Paolisso, Giuseppe, et al. "Pharmacological doses of vitamin E and insulin action in elderly subjects." The American journal of clinical nutrition 59.6 (1994): 1291-1296.
  • Salonen, Jukka T., et al. "Increased risk of non-insulin dependent diabetes mellitus at low plasma vitamin E concentrations: a four year follow up study in men." Bmj 311.7013 (1995): 1124-1127.
  • Stattin, Pär, et al. "Prospective study of hyperglycemia and cancer risk." Diabetes care 30.3 (2007): 561-567.
  • Uchida, Tomono, et al. "α-Tocopherol does not Accelerate Depletion of γ-Tocopherol and Tocotrienol or Excretion of their Metabolites in Rats." Lipids 48.7 (2013): 687-695.
  • Vivekananthan, Deepak P., et al. "Use of antioxidant vitamins for the prevention of cardiovascular disease: meta-analysis of randomised trials." The Lancet 361.9374 (2003): 2017-2023.

Saturday, April 26, 2014

True or False: Xanthan Will Reduce The Glycemic Index of Your Meals, Increase Satiety and Have an Overall Beneficial Effects on Your Metabolic Health (Glucose, Lipids, Waist, ...)

Can xanthan reduce the glycemic response to "sweet treats" like this?
Have you ever heard of xanthan? Yep that's E-number E415. What? If it has an E-Number it can't be good? Well, what about vitamin C, then? That's E-Number E300. Does this make it "bad" for you? If so, I'd suggest you skip today's SuppVersity article and avoid xanthan out of principle. Otherwise, I would like to offer you to join me for another "True or False" Session (find more of these | RSS-compatible browser or plugin for Chrome like SlickRSS needed) at the end of which we will know whether the statement "Xanthan Will Reduce Your Meals Glycemic Index, Increase Satiety and Have Overall Beneficial Effect on Your Metabolic Health" is true, or false.
You can find more True or False articles at the SuppVersity

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High Volume Diet = Success
When it's added to juice (alongside with beta-glucans), xanthan will reduce the glucose response and thus help stabilize blood sugar levels (Paquin. 2012).

Figure 1: Mean (S.E.) changes of hunger, fullness, desire to eat, and prospective consumption after ingestion of 325 ml of a thin and thick shake. Ratings were provided on nine-point category scales. “*” indicates a significant difference in ratings for the two shakes (Mattes. 2001).
The stabilized blood sugar levels, in turn, will will eventually have beneficial effects on 24h satiety.

This goes, even though Julie Paquin and her colleagues did not detect an acute increase in their 2012 study on the effects of xanthan and β-glucan enriched juices on the glycemic response and satiety of healthy men. Previous studies suggest that the viscosity of a liquid meal, which is increased by the addition of xantham, may be an important determinant of the hunger response.

Mattes and Rothacker (2001), for example reported significantly greater and more prolonged reductions in hunger with thicker, but otherwise identical replacement shakes.

Marciani et al. (2001) even found that the viscosity of their high- vs. low-viscosity shakes with different macronutrient and energy content had a greater impact on the satiety than the fat, carbohydrate or energy content of the test meals.
Food Volume Matters!
SuppVersity Suggested Read: "True or False: High Volume + Nutrient + Low Energy Foods Keep You Lean. Bonus-Question: Will a High Volume Make Your Stomach Go Baggy & Mess Up Your Satiety Response?" | read more - Just in case you've already forgotten that I've covered the beneficial effects of a "high volume, high nutrient, low energy" diet and the corresponding increase in gastric volume in one of the last installments of the True or False Series | go trough previous installments.
The scientists from the University Hospital, Nottingham were also able to show a direct correspondence between the gastric volume of the viscous meal ad the satiety response. These observations support the dual hypothesis, i.e. that more viscous fibres exert their effect owing to distention in the gastric antrum and/or altered transport of nutrients to the small intestine, Caroline Hoad et al. put forward in their 2004 paper in the Journal of Nutrition (Hoad. 2004).

Table 1: Viscosity AUC values for solutions containing select dietary fibers during gastric digestion simulation
In view of the fact that a comparison of the total viscosity per gram of 12 different fiber types Dikeman et al. published in the Journal of Nutrition in April 2006 indicates that xanthan has by far the highest viscosity of all 12 tested types of dietary fiber (Dikeman. 2006), it appears to be certain that the polysaccharide, which is secreted by the bacterium Xanthomonas campestris, will exert significant beneficial effects on both the volume of a given liquid meal and the time it takes to pass through the digestive tract - and this will, as we have just learned, improve fullness and satiety, and decrease the energy intake of every dieter.
Why does glycemia even matter? Aside from the fact that extreme glucose excursions after a meal are partly responsible for the development of diabetes, avoiding them will (1) stabilize your energy levels and curb your cravings, (2) decrease inflammation and oxidative stress, (3) help you maintain healthy blood lipid and body fat levels, (4) reduce your cancer and heart disease risk, and so on. You see, if xanthan can help you stability your blood sugar levels, this alone would have a long string of beneficial health consequences.
At this point, I could probably cite the dirty dozen of studies that support the appetite suppressing effects of PGX®, a combination of xanthan, sodium alginate and glucomannan (e.g. Jenkins. 2010; Tao. 2010; Kacinik. 2011; Reichert. 2013).
Figure 2: Postprandial glycemia in healthy subjects after the consumption of various breakfast meals (Jenkins. 2008) similar beneficial effects in response to the addition of a 70% glucomannan and 30% xanthan blend to the buiscuits were observed in diabetic subjects, as well.
In view of the fact that we are interested in the individual effects of xanthan, and not in the promotion of an expensive, albeit scientifically proven fiber supplement where xanthan is only one (but probably one of the most important) ingredients, I will leave the PGX-related evidence behind and turn to "xanthan only" studies to substantiate my assertion that xanthan gum is a beneficial, albeit not necessary, addition to the dietary regimen of both, lean and overweight physical culturists.
Warning! Xanthan is safe for adults (Eastwood. 1987), but probably not safe for infants. This is at least what a report from the US Food and Drug Administration in the Journal of Pediatrics would suggest (Beal. 2012). According to the USDA, the potential for thickened feeds to increase risk of necrotizing enterocolitis (NEC), a leading cause of morbidity and mortality in neonates, has not been thoroughly assessed. Nevertheless, the occurrence of 202 cases of NEC in formula-fed (obviously) infants over 12 years should yet be reason enough to keep your xanthan stash far away from your newborn, irrespective of the fact that the case series Beal et al. present cannot prove an association between the xanthan-containing thickening agent SimplyThick and NEC.
Odutola Osilesi and colleagues from various US Universities and the USDA were among the first to propose and demonstrate the potential usefulness of xanthan gum in dietary management of diabetes mellitus (Osilesi. 1985). In the corresponding experimental trial, they supplied 9 drug-free diabetics with moderately elevated serum glucose and four nondiabetic controls controls with - you guessed it - muffins that contained 12g of xanthan gum.
Figure 3: Muffins w/ 12g xanthan/day have significant beneficial effects on glucose management in diabetics and beneficial, but non-significant effects on fasting and post-prandial blood sugar in healthy subjects (Osilesi. 1985)
The subjects were randomly assigned to to a "xanthan first" or "control first" group for 2x six weeks. Before the study and at the end of the xanthan and xanthan-free periods, the scientists analyzed the blood before and 2 h after an oral glucose load.

Figure 4: Effect of the guar (G), xanthan (X), locust bean gum (LBG), and 1: 1 mixtures of X and LBG (X/LBG) and X and Meyprodyn (X/Mey) on the movement of radiolabeled glucose in the mixture (concentrations in % | Edwards. 1987)
You can see the results of this undertaking in Figure 4. Basically, what the researchers found were...
  • significant reductions in fasting and postload serum glucose and reduced fasting levels of total plasma cholesterol in diabetic subjects, as well as
  • lower fasting and postload levels of gastrin and gastric inhibitory polypeptide (GIP) and fasting levels of total and VLDL triglyceride and cholesterol in VLDL and LDL fractions
Moreover, all subjects reported a sense of fullness after consuming xanthan muffins but no severe digestive symptoms. The latter will usually become more prevalent, when xanthan is mixed with other fibres like galactomannan in a (successful) effort to promote its anti-cholesterol effect (Yamamoto. 2000).

In view of the fact that mixing with (obviously) lower viscosity fibers will not necessarily increase the hypoglycemic (glucose improving) effects, of which Edwards et al. (1987) demonstrated that they depend almost exclusively on the viscosity of the chyme, it appears unwarranted to spend the extra bucks on galactomannan or other fibers... Unless you are battling high cholesterol levels and would like to see a similar beneficial effects on your blood lipids as the rodents in the Yamamoto study, of course.
Yes, xanthan will increase satiety and have beneficial effects on glucose metabolism. Whether it is a "necessary" addition to everyone's diet, on the other hand, is questionable. It's a supplement and supplements are, as their name implies "supplemental".

A single teaspoon will already make a protein shake really thick! And remem- ber: more xanthan = high viscosity = slow gastric passage, high satiety, but slow nutrient release
There are, moreover, also situations, where you may not even want to reduce the transit of a liquid meal through your digestive tract. After a workout, for example, xanthan should be used only people who go hypogylcemic in response to the whey (+sugar) induced insulin spike in response to their post-workout shake.

As part of a high protein snack, on the other hand it does really make sense to combine xanthan, whey and maybe some resistant starch (RS4) into a energy-laden power-"shake"... just be careful: If you use more than a teaspoon your "shake" will easily turn into a pudding and you can spoon-feed yourself a fluffy protein pudding ;-)
Reference:
  • Beal, Jennifer, et al. "Late onset necrotizing enterocolitis in infants following use of a xanthan gum-containing thickening agent." The Journal of pediatrics 161.2 (2012): 354-356.
  • Dikeman, Cheryl L., Michael R. Murphy, and George C. Fahey. "Dietary fibers affect viscosity of solutions and simulated human gastric and small intestinal digesta." The Journal of nutrition 136.4 (2006): 913-919. 
  • Edwards, C. A., et al. "Viscosity of food gums determined in vitro related to their hypoglycemic actions." The American journal of clinical nutrition 46.1 (1987): 72-77.
  • Eastwood, M. A., W. G. Brydon, and D. M. W. Anderson. "The dietary effects of xanthan gum in man." Food Additives & Contaminants 4.1 (1987): 17-26.
  • Hoad, Caroline L., et al. "In vivo imaging of intragastric gelation and its effect on satiety in humans." The Journal of nutrition 134.9 (2004): 2293-2300.
  • Jenkins, Alexandra L., et al. "Comparable postprandial glucose reductions with viscous fiber blend enriched biscuits in healthy subjects and patients with diabetes mellitus: acute randomized controlled clinical trial." Croatian medical journal 49.6 (2008): 772.
  • Jenkins, Alexandra L., et al. "Effect of adding the novel fiber, PGX®, to commonly consumed foods on glycemic response, glycemic index and GRIP: a simple and effective strategy for reducing post prandial blood glucose levels-a randomized, controlled trial." Nutrition journal 9.1 (2010): 58.
  • Kacinik, V., et al. "Effect of PGX, a novel functional fibre supplement, on subjective ratings of appetite in overweight and obese women consuming a 3-day structured, low-calorie diet." Nutrition & diabetes 1.12 (2011): e22.
  • Marciani, Luca, et al. "Effect of meal viscosity and nutrients on satiety, intragastric dilution, and emptying assessed by MRI." American Journal of Physiology-Gastrointestinal and Liver Physiology 280.6 (2001): G1227-G1233.
  • Mattes, Richard D., and Dana Rothacker. "Beverage viscosity is inversely related to postprandial hunger in humans." Physiology & Behavior 74.4 (2001): 551-557.
  • Osilesi, Odutola, et al. "Use of xanthan gum in dietary management of diabetes mellitus." The American journal of clinical nutrition 42.4 (1985): 597-603.
  • Paquin, Julie, et al. "Effects of juices enriched with xanthan and β-glucan on the glycemic response and satiety of healthy men." Applied Physiology, Nutrition, and Metabolism 38.4 (2012): 410-414.
  • Reichert, Ronald G., et al. "Meal replacements and fibre supplement as a strategy for weight loss. Proprietary PGX® meal replacement and PGX® fibre supplement in addition to a calorie-restricted diet to achieve weight loss in a clinical setting." Biotechnology and Genetic Engineering Reviews 29.2 (2013): 221-229. 
  • Tao, Wendy. "A clinical observational study on PGX® conducted at the Canadian Centre for Functional Medicine." Alternative Medicine Review (2010) 15.1: 68-75.
  • Yamamoto, Yukiko, et al. "Improved hypolipidemic effects of xanthan gum-galactomannan mixtures in rats." Bioscience, biotechnology, and biochemistry 64.10 (2000): 2165-2171.