BCAA's enhance ketosis on a ketogenic diet

[hailtotheking]

This is quite a good presentation on how BCAA and a ketogenic diet are synergistic.

http://www.pepck-and-the-ketogenic-d...geliouBCAA.pdf

I didnt understand it fully, but its basically down to the fact that the overall effect of the amino acids in BCAAs are ketogenic, so can actually enhance ketosis, whilst enabling greater nitrogen retention than a standard low protein clinical ketogenic diet.

Basically it enables the maintenance of the Ketogenic Ratio but with a simulated higher protein intake, which is something physique-oriented folks maybe interested in, and could possibly enable muscle gain on a ketogenic diet.

Combined with the MCT version of the Ketogenic diet (which allows even higher protein intake), its an interesting concept.

[hailtotheking]

There is more here on the use of BCAAs on the MCT Ketogenic Diet

Perfect Health Diet » Ketogenic Diets, I: Ways to Make a Diet Ketogenic
Perfect Health Diet » Ketogenic Diets 2: Preventing Muscle and Bone Loss on Ketogenic Diets

I thought about if EAAs would work just as well, but unfortunately it seems that supplemental EAAs would probably hinder ketosis because within the EAAs there are more glucogenic AAs than ketogenic ones.

[Ben_S]

HTTK and Nu,

What are your thoughts on this article?:

Perfect Health Diet » Dangers of Zero-Carb Diets, II: Mucus Deficiency and Gastrointestinal Cancers

Worrying me a bit!...

[James]

Super post man, very interesting reads. I will be switching back to a keto style diet once I pack on the desired size and get to my genetic ceiling, so this makes superb reading.

[NU_nutrition_TS]

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HTTK and Nu,

What are your thoughts on this article?:

Perfect Health Diet » Dangers of Zero-Carb Diets, II: Mucus Deficiency and Gastrointestinal Cancers

Worrying me a bit!...

I thought it was a pretty 'weak' argument when I first read it but others (qualified) have thoroughly debunked it since! You cannot have a zero carb diet anyway, the lowest you are ever likely to get is around 10g per day.

[Ben_S]

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I thought it was a pretty 'weak' argument when I first read it but others (qualified) have thoroughly debunked it since! You cannot have a zero carb diet anyway, the lowest you are ever likely to get is around 10g per day.

Great news! Do you possibly have a link to said debunking please NU?

[NU_nutrition_TS]

I was trying to locate it while posting my reply (above) but had no luck. However here is a relevant part of a debunking (or refutation) of Jaminet's position by Dr. Ron Rosedale (Jaminet's remarks are in quotes [""] followed by Dr Rosedale's responses):

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“the biggest reason for glucose utilization is the construction and maintenance of the human glycome [for immune, mucous etc.]“

Again, no one is disputing the fact that glucose is a necessary nutrient. We’re just disputing the necessity of eating it.

“Why, if cells can run on glucose and blood glucose remains normal, do starving people die?”

Because maybe most of the cells are not meant to run on glucose, but rather ketones, and a person will die when fat stores and precursors to ketones are insufficient.

“A clue [about glucose deficiency] is the fact that starving people develop a hacking cough in their final weeks of life. Despite blood glucose levels in the normal range, they cease producing mucus…”

Starving people are protein deficient much more than glucose deficient, and mucin is a glycoprotein…and a protein deficiency affects much more than the mucous per se. including the membranes themselves, including innervation to those membranes, blood circulation to those mucous membranes that shuts down secondary to vascular dysfunction and intravascular volume depletion secondary to reduced albumin/osmolarity, and heart failure…and so many other functions that only time would limit talking about. At that point, giving a gallon of glucose probably wouldn’t help. That person needs protein and fat.

Also, you are equating a person starving and near-death, and running out of all energy substrates to stay alive, to one on a high fat, very low carbohydrate diet that evidence reveals may extend lifespan–Not quite appropriate.

Incidentally, the body preferentially maintaining blood glucose until the end reveals the vital importance of having an anaerobic fuel supply available for fight and flight emergencies. That is main reason we keep glucose around.

“The reality is this: peripheral glucose utilization is not determined by blood glucose levels, but is hormonally regulated.”

Correct, except for those tissues in which glucose entry is not regulated by hormones and where most of the damage occurs from that glucose, the endothelium to name an example. Furthermore, the hormones that do determine glucose utilization are in turn strongly influenced by glucose levels.

“What are the hormones that regulate glucose utilization? During glucose deficiency, T3 thyroid hormone levels decrease and reverse-T3 levels increase.”

I believe that Jaminet and most others misunderstand the physiologic response to low glucose, and the true meaning of low thyroid. Glucose scarcity (deficiency may be a misnomer) elicits an evolutionary response to perceived low fuel availability. This results in a shift in genetic expression to allow that organism to better survive the perceived famine. Intracellular antioxidant systems, heat shock proteins, DNA repair, autophagy, all tricks that nature has, are up-regulated to allow the organism to increase repair and maintain itself to remain healthy and alive. As part of this genetic expression, and as part and parcel of nature’s mechanism to allow the maintenance of health and actually reduce the rate of aging, certain events will take place as seen in caloric restricted animals. These include a reduction in serum glucose, insulin, leptin, and free T3.

The reduction in free T3 is of great benefit, reducing temperature, metabolic damage and decreasing catabolism. TSH is not elevated. We are not talking about a hypothyroid condition. It is a purposeful reduction in thyroid activity to elicit health. Yes, reverse T3 is increased, as this is a normal, healthy, physiologic mechanism to reduce thyroid activity. It is not always a sign of malfunctioning thyroid as is frequently taught, but is instead one of the redundant ways that thyroid action is controlled. Reduced thyroid level in this regard is analogous to reduced fasting insulin that generally indicates improved insulin sensitivity, which also occurs in fasting and caloric restricted animals, and is also part and parcel of the benefits seen. Sometimes our complexity is indeed paradoxical.

“Decreased production of molecules like hyaluronan and mucin and reduced levels of T3 thyroid hormone, then, are outcome of dietary glucose deficiency.”

Reduced levels of T3 occur secondary to leptin reduction that occurs secondary to reduction in glucose. This is not a detriment and is not hypothyroidism, but part and parcel of genetic expression of increased maintenance and repair. See above. As far as ‘glucose deficiency’ impairing mucin and hyaluronan production; I respect your theory but cannot agree with it as it lacks evidence, nor do I agree with the concept of glucose deficiency while on a VLC diet such as mine (moderate protein, relatively high fat).

“Do Glucose Deficiency Symptoms Actually Occur in Low-Carb Dieters?
Yes.”

No. There is no such thing as a glucose deficiency until one is dead or nearly so…There can be a glycosylation deficiency secondary to improper instructions about what to do with glucose often secondary to glycation and improper insulin and leptin signaling at least partially contributed to also by excess glucose. Glucose deficiency is not the same as glycosylation defects or deficiencies. Again, it is not a lack of glucose but signals that tell us what to do with it that are most critical.

“…many cases of glucose deficiency symptoms that developed on very low-carb Paleo or GAPS diets…”

It is a big jump to assume that problems were due to ‘glucose deficiency’. Were these people substituting high protein or beneficial fats for carbs…big difference?… Did they supplement with magnesium and potassium and other nutrients that are necessary when instituting a very low carbohydrate diet secondary to a fall in insulin and the diuresis of retained fluid. There are so many variables that are not accounted for here, that jumping to the conclusion that it is a glucose deficiency is not warranted.

Also, testimonies will be forthcoming from any diet, healthy or otherwise…just look at any infomercial. After using my very low-carbohydrate moderate protein and sufficient fat to satisfy hunger and energy needs diet, and after having reversed countless numbers of diabetics, including several T1s, heart failure patients, hypertensives, and even a few severe metastatic cancer patients, I could furnish a few testimonies of my own that time, space, inclination, and relevance precludes from printing here…and I have never heard of a mucus deficiency problem on my diet.

“Low-carb diets, alas, impair immunity to fungal and protozoal infections.”

Quite debatable. Fungi in particular feed on sugar and many books have been written attributing considerable success in treating fungal infections to glucose restriction.

“The Possibility of Slow-Developing Problems Cannot Be Ruled Out”

Certainty does not exist. However, the possibility, even probability of slowly developing problems can be likely ruled in secondary to dietary intake of glucose forming starches such as rice and potatoes i.e. glycation, serum elevations in insulin and leptin, etc.

“Biomedical researchers are gradually realizing the importance of glycosylation defects in leading diseases. I report these papers, not because I think they tell us how many carbohydrates we should eat – they don’t – but to remind everyone of the complexity of biology.”

Yes, these papers are not very relevant to our discussion, but yes, it is good to point out the complexity of biology, however that complexity is more complex than indicated Just eating more carbs will not fix that GnT4a deficiency.. It would need to be genetically expressed, and non-enzymatic glycation resulting from increasing BG secondary to potato and rice consumption will, if anything, hinder that.

Believing that a glucose deficiency is behind mucus, immune, cancer and diabetes problems, is a huge leap, and is analogous to believing that most cases of osteoporosis is secondary to calcium deficiency in Western society. It is not a problem with the pieces. In nearly all of these cases we have enough of those. The problem lies in how we are putting them together, and this is hormonally controlled, and the most influential of these hormones are nutrient sensors controlled by diet that glucose consumption corrupts. It is far, far more likely for glycosylation defects to occur secondary to (non-enzymatic) glycation, than from lack of glucose.

“We cannot be sure that there may not be negative health effects from severe carb restriction that will show up only after decades.”

Well, so far they have not been found. That is why carbohydrates are a nonessential nutrient.

“I think everyone should acknowledge that very low-carb diets may have unexplored risks.”

We can say that about any diet, and in fact any event. One can only use the best science available and make the best guess available. We do know one thing for sure, a high carbohydrate diet is a major cause of all chronic disease. I see nothing wrong in running the other way.

His full response is here: More ‘Safe Starches’ Stuff And Why I’ve Decided NOT To Test Them On Myself « Jimmy Moore's Livin' La Vida Low Carb Blog

[NU_nutrition_TS]

Also this:

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First, I read his linked reference about defects in O-glycosylation that he listed in his blog (regarding cancer and dysbiosis) as supporting his recommendations for adding carbs as a source of glucose to reduce the impact of an O-glycosylation defect.

If you read the paper you see that O-glycosylation defects have been associated with the cancer phenotype and alterations in mucin production in the gut. They are important for mucin production and he mentions that. However, that paper is more about scientific findings that suggest that the quartenary structure of glycosylation enzyme complexes are much more efficient than activity of the same unassociated enymes. I’m not sure what this has to do with his recommendation to avoid a glucose (and ? hence glycosylation) deficiency by consuming large amounts of glucose. If anything, this type of diet can enhance HbA1c which is glycosylated hemoglobin!

As you well know, when an enzyme acts on a substrate (such as an enzyme that adds a sugar molecule to an enzyme side chain — as discussed in his reference) the pathway involves the action of an enzyme on a substrate (here the sugar molecule). The defects in glycosylation that the researchers are referring to involve decreases in enzyme activity, not deficiencies in available substrate (such as glucose). Usually in biological reactions of this type there are literally billions of sugar molecules available, so lack of substrate is rarely an issue. The main problem is inactivity of the enzyme itself, which is not impacted by how much sugar is available. So suggesting that we eat high glucose to avoid a glycosylation problem doesn’t have any scientific validity, in my opinion.

DR. LARRY MCCLEARY, AUTHOR OF FEED YOUR BRAIN LOSE YOUR BELLY, from here: Is There Any Such Thing As ‘Safe Starches’ On A Low-Carb Diet? « Jimmy Moore's Livin' La Vida Low Carb Blog

It should be noted that Paul Jaminet is an astrophysicist, so his field of expertise is not nutrition. That fact, in itself, is not necessarily a reason to dismiss his dietary recommendations but it does indicate that he may not always fully understand or appreciate the nuances of the nutritional scientific literature he cites to support those recommendations.

[hailtotheking]

I personally favour Chris Masterjohn's view that if protein OR carbs OR a mix of both is sufficient on a high fat diet than there's probably nothing to worry about in terms of adequate glucose availability. I.e if protein intake is sufficient but carbs are really low, then gluconeogeneis will probably create adequate glucose.

The observation that there seems to be an increased rate of stomach cancer among very low carbers (e.g those on the Optimal Diet plan) was discussed a bit more here http://high-fat-nutrition.blogspot.c...acid-post.html. CarbSane suggests another possible mechanism might be lack of certain sugars to feed required gut bacteria.

Nu, i find Rosedale's assumptions about low free T3 and high reverse T3 being good for us a bit incredulous. Several people in my family have sub-normal range Thyroid hormone levels and would probably want to slap anyone who suggested its a good condition to have, and if Rosedale's suggestions were correct then i would expect to see a decreased mortality rate among hypothroidism sufferers.

Jaminet has replied in detail to all of Rosedale's comments on this matter http://perfecthealthdiet.com/?cat=145

[NU_nutrition_TS]

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Nu, i find Rosedale's assumptions about low free T3 and high reverse T3 being good for us a bit incredulous. Several people in my family have sub-normal range Thyroid hormone levels and would probably want to slap anyone who suggested its a good condition to have, and if Rosedale's suggestions were correct then i would expect to see a decreased mortality rate among hypothroidism sufferers.

You have to take what he said in context:

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The reduction in free T3 is of great benefit, reducing temperature, metabolic damage and decreasing catabolism. TSH is not elevated. We are not talking about a hypothyroid condition. It is a purposeful reduction in thyroid activity to elicit health. Yes, reverse T3 is increased, as this is a normal, healthy, physiologic mechanism to reduce thyroid activity. It is not always a sign of malfunctioning thyroid as is frequently taught, but is instead one of the redundant ways that thyroid action is controlled. Reduced thyroid level in this regard is analogous to reduced fasting insulin that generally indicates improved insulin sensitivity, which also occurs in fasting and caloric restricted animals, and is also part and parcel of the benefits seen. Sometimes our complexity is indeed paradoxical.

Reduced levels of T3 occur secondary to leptin reduction that occurs secondary to reduction in glucose. This is not a detriment and is not hypothyroidism, but part and parcel of genetic expression of increased maintenance and repair. See above.

I think he was quite clear to separate what he sees as a healthy compensation from a pathological, symptomatic condition.

I have also argued that thyroid hormone levels currently classed as 'normal' (actually a misnomer because they are 'usual' or 'commonly seen in the majority of cases' on lab tests) are so defined when observed through the lens of the prevailing 'Western diet' (high carb). That in itself does not guarantee that they are normal or healthy any more than lower levels on a low carb diet indicate any abnormality. They are just different and reflect metabolic adaptation. Most people suffering from a pathological, symptomatic thyroid problem (whether under or over active) are also usually eating the prevailing 'Western high carb diet' as those who have 'normal' or 'usually seen' levels, so diet, in and of itself, must be secondary (if related at all) to these types of dysfunction.