Here you will find list of products which are low in carbohydrates and should constitute the basis of  your diet. If you will exclude starch from your diet that would be already a very big step in the way to get better.
This list  doesn’t show obvious products high in sugars like starch, sweets, sodas and fast food.
Our goal is to create an inspiring page for people who, like us, have high insulin or diabetes, yet still want to enjoy the treats in life.
Matt Farina is in the process of using the Perfect Health Diet to recover from hypothyroidism, and wanted to report his progress to PHD readers. The doctor asked if I had any of the common symptoms of hypothyroidism; I said I was tired in the day and had brain fog in the morning. I decided to start researching causes and cures of hypothyroidism, and started to listen to podcasts from Ben Greenfield and Robb Wolf.
In May 2014, I sent Ben Greenfield an email saying I was considering starting a Paleo diet to overcome my hypothyroidism and I really wasn’t expecting a reply considering how busy he must be. I decided that I would stick with the 50 mcg dose of levothyroxine, and see if diet could help me. The first 3 months on the Perfect Health Diet yielded weight loss and other health benefits. After 3 months on the Perfect Health Diet, in late August 2014, I had a set of blood tests.
At my 12 month anniversary of adopting the Perfect Health Diet, in June 2015, I was tested again.
The doctor suggested cutting my levothyroxine dose in half, to 25 mcg per day, but I’ve decided to drop levothyroxine entirely and see if I show hypothyroidism symptoms. I fully intend to continue the Perfect Health Diet indefinitely, and I hope my story helps other people overcome their hypothyroidism. Back in May 2014, when I first learned about PHD and the hope that it gave for natural thyroid healing, and heard my doctor say that hypothyroidism was genetic and incurable and that I would be living with it for the rest of my life, I left the doctors office feeling sad. In Part I of this series, I reviewed the biology of Neu5gc (“Neu5gc, Red Meat, and Human Disease: Part I,” January 14, 2015). Neu5gc is abundant in nearly all mammals, but is absent in humans, ferrets, and new world monkeys.
Although humans cannot manufacture Neu5gc due to a mutation that occurred 3 million years ago, we retain the ability to utilize it.
To generate a broad-spectrum immune response, the DNA of B cells is re-arranged to create novel combinations of segments on the light- and heavy-chain portions of antibodies.
So Neu5gc has the potential to accumulate in human cells, especially intestinal cells which are directly exposed to food; and we can form antibodies to Neu5gc, which then may react to human cells which have incorporated Neu5gc into their carbohydrate coat. Bacteria are potent immunogens because they express a number of factors that can act as immune stimulants. So to generate autoimmunity against Neu5gc incorporated in human cells, B cells must first be triggered to form high-affinity anti-Neu5gc antibodies by meeting bacterial pathogens who have incorporated Neu5gc into their cell walls.
This can happen because some bacteria do incorporate sialic acids from their local environment into their cell walls; and thus gut bacteria will incorporate Neu5Gc from food into cell walls.
A primary reason for doing this is that, by coating themselves in sialic acids acquired from their host, they look like a “host cell” and are shielded from immune attack. Many pathogens secrete a sialidase that releases sialic acid from [nearby cells] … [O]ther sialic acid-utilizing bacteria, such as the respiratory pathogen H.
Among the pathogens known to use host sialic acids to shield themselves from human immunity is Neisseria gonorrhoeae, the pathogen that causes gonorrhea. To date, the published research on this topic has focused on the possibility of pathogens incorporating Neu5Ac, the primary human sialic acid, from human cells into their cell walls, and subsequently triggering autoimmunity against Neu5Ac. Yet a recent study [4] comparing the levels of Neu5Gc antibodies in human blood against the prevalence of Hashimoto’s hypothyroidism suggests that this may be a significant pathway for autoimmunity. They also tested for anti-Neu5Gc antibodies in rheumatoid arthritis patients, but found no connection there. I suffered badly with childhood asthma, and I still get a sort of asthmatic tightness of my breathing once in a while.
When an upsurge of titer of anti-Neu5Gc antibodies float in body fluids, they have opportunity cause inflammatory reaction. My own experience is I develop a groin ‘heat rash’ type reaction and irritable bladder a day or so after eating too much cheese and red meat.
Jim’s personal experiences add further evidence that Neu5Gc-driven inflammation and autoimmunity is a real phenomenon.
An infection in the gut by bacterial pathogens that acquire Neu5Gc from food (primarily beef and pork) and incorporate it into their cell walls. Significant consumption of beef and pork, providing the Neu5Gc to drive the autoimmune process. Reducing dietary Neu5Gc by replacing beef, dairy, lamb, and pork with seafood and bird meats. Neu5Gc-mediated autoimmunity does not play a role in rheumatoid arthritis, but it may play a role in other autoimmune diseases.
We have a few spots remaining for the May 2-9 Perfect Health Retreat, and will soon be taking reservations for the October retreat, either October 3-10 or 10-17 (or both). One of the more mysterious conditions afflicting low-carb Paleo dieters has been high serum cholesterol. On the first post, one of the causes suggested by readers was hypothyroidism – an astute answer. Weight loss (and VLC diet) resulting in hypothyroidism resulting in elevated cholesterol due to less pronounced LDL receptors?
Those answers caused me to put the connection between hypothyroidism and LDL levels on my research “to do” list. Chris Masterjohn has done a number of blog posts about the role of LDL receptors in cardiovascular disease. So higher T3 = more LDL receptors = more LDL particles pulled into cells and stripped of their fatty cargo. If LDL particles were being taken up from the blood via LDL receptors, they would have to be replaced – a resource-expensive operation – or immunity would suffer. Suppose LDL receptors are so thoroughly suppressed by low T3 that the lipid transport function of LDL is abolished.
So, if T3 hormone levels are very low and there is an infection, LDL particles will get oxidized and cleared by immune cells, and LDL levels will stay low. If LDL particles continue to be generated, which happens in part when eating fatty food, then LDL levels might increase. A chronic state of glucose deficiency, leading to very low T3 levels and suppressed clearance of LDL particles by lipid transport pathways. Absence of infections or oxidative stress which would clear LDL particles by immune pathways.
Alternatively, there is evidence that some infections may induce euthyroid sick syndrome, a state of low T3 and high rT3, directly. One of the claims of low carb dieting is that it will normalize the symptoms of metabolic syndrome. I went very low carb in April in an effort to address metabolic issues, eating as little as 15grams carbohydrate per day. I had expected triglycerides and cholesterol to drop when I cut the carbs, but they did the opposite: They surged.
Saturated fat: The increase in saturated fat created a superabundance of cholesterol which the liver cannot handle.
Temporary hyperlipidemia: The surge in lipids is the temporary consequence of the body purging visceral fat.
Hibernation: The metabolism has gone into “hibernation” with the result that the thyroid hormone T4 is being converted into rT3, an isomer of the T3 molecule, which prevents the clearance of LDL. When a person experiences prolonged stress, the adrenals manufacture a large amount of the stress hormone cortisol.
In case the malnutrition explanation was a factor, I began supplementing copper and eating my wife’s delicious liver pate three times per week. The rT3 theory is elegant and I was eager to test my claim that the bulk of the cholesterol was due to a problem with clearance rather than ‘superabundance’. My current goal is to address the root causes of the rT3 dominance and wean myself off the T3 supplement. Preparation: In order to tolerate T3 supplement you have to be sure that your iron level and your adrenals are strong enough. Practicalities: T3 supplementation requires daily temperature monitoring in order to assess your progress. As Chris Masterjohn said, in the quote above, if you are going to do very low carb, check your thyroid levels.
I also think my experience may help prove thyroid hormone replacement to be an alternative, and superior, therapy to statins for very high cholesterol. However, I would be very reluctant to recommend T3 supplementation as a treatment for high LDL on Paleo.  If the cause of low T3 is eating too few carbs, then supplementing T3 will greatly increase the rate of glucose utilization and aggravate the glucose deficiency. The proper solution, I think, is simply to eat more carbs, to provide other thyroid-supporting nutrients like selenium and iodine, and allow the body to adjust its T3 levels naturally. GB: What if one is glucose intolerant and can’t tolerate more than 60 grams per day without hyperglycemia or weight gain?
Finally, if I may sound like Seth Roberts for a moment, I believe this story shows the value of a new form of science: personal experimentation, exploration of ideas on blogs, and the sharing of experiences online.


Now it’s time to look more closely at the evidence to see if my perspective is consistent with the literature. Mario had assistance from JS Stanton of gnolls.org who reviewed the post pre-publication and contributed some helpful suggestions. After my post on low carb diets and thyroid function, Anthony Colpo wrote a reply that I will address with this post. Second, Anthony has been making a case that low-carb diets can produce a condition called “euthyroid sick syndrome,” characterized by low T3 and high rT3. In the developed world, most cases of hypothyroidism – up to 90% – are diagnosed as Hashimoto’s autoimmune thyroiditis.
Which infections are associated with Hashimoto’s is still an object of study, but we do know that many of the likely pathogens benefit from high gut, serum, or cellular glucose levels  and therefore we can suspect that a high carbohydrate diet might promote the disease and a low, but not too low, carbohydrate diet, such as PHD, might be therapeutic. So even if some thyroid-related problems, like euthyroid sick syndrome, may become more likely on a low-carb diet, others, like Hashimoto’s, may be relieved by a low-carb diet. In looking at the papers cited by Anthony, I’ll borrow his section headings so that readers have an easier time finding the part of his post that I am responding to. Anthony, in an attempt to refute my assertation that PUFA may cause thyroid impairment on LCHF diets, cites two papers. However, as you scan through the above paper, you will notice that one of the groups followed a zero-carb diet consisting of nothing but lean meat, fish, fowl, and vitamin and mineral supplements. In short: On a 7-day modified fast providing 130 protein calories per day, the fall in T3 levels is significantly less than on a 7-day true fast. Apparently, isocaloric carbohydrate deprivation induces a catabolic state with respect to protein metabolism compared with diets with a normal composition and compared with starvation.
The subjects in the Volek study were asked to maintain their current level of physical activity and to consume adequate dietary energy to maintain body mass.
Lesson: if you don’t want to lose muscle on a VLCD, eat extra protein and at least a bit of carbs! The study headed by Jeff Volek  is the only one allegedly showing no change in thyroid hormone levels on a low-carb diet, so of course it is eagerly cited by Mario as proof that I’m wrong. This, of course, is just fine by Mario, who happily extrapolates the results of unrelated studies examining the relationship between thyroid hormones and a bunch of other hormones; studies, I should point out, that did not involve low-carb diets. Paul has argued that gluconeogenesis is hormonally limited and can generate at most 400 glucose calories per day; this is why zero-carb diets are dangerous. What is interesting about Otten et al is that the diet of 50% carbohydrate and 50% fat showed a decrease of 24% in T3 and an increase of 34% in rT3.
As anticipated, total fasting resulted in a 53% reduction in serum T3 in association with reciprocal 58% increase in rT3. Mario and Stabby jump on this finding as if it is proof that only fifty grams of carbohydrate is needed to maintain optimal carbohydrate levels. Based on Paul’s view of things, it would be no surprise that this was not a universal finding. But it is significant that when circumstances are right, 200 calories per day of carbs can eliminate the T3 drop and rT3 rise that is associated with glucose deficiency.
Anthony cited several other studies in which 200 carb calories was insufficient to prevent a rise in T3. Recall that Paul believes that 200 carb calories and 600 calories of carb+protein are the bare minimum needed to prevent a glucose deficiency, even when all circumstances are favorable. Average carbohydrate intake in grams was 250 grams on the standard diet, 71 grams on the low-carbohydrate diet, and 533 grams on the high-carbohydrate diet. Finally, Anthony cited a study by Davidson and Chopra [8] which found that T3 levels increased as carbohydrate intake increased from 20% toward 80% of energy. However, there is as yet no evidence that T3 and rT3 will exit normal ranges when following Perfect Health Diet guidelines. Until a well-designed study provides contrary evidence, I stand by my assertion that a diet with sufficient but not excess protein, moderate carbohydrate comprising a minority of calories, and high intake of saturated and monounsaturated fat but low intake of polyunsaturated fat is optimal for thyroid function. Come to the Perfect Health RetreatCome join us for a week at the beach learning how to achieve a lifetime of great health! Buy our bookPerfect Health Diet: Regain Health and Lose Weight by Eating the Way You Were Meant to Eat is a great way to understand the dietary and nutritional practices that lead to optimal health. AOBiome Skin ProbioticsWe recommend AOBiome's AO+ Mist skin probiotics, which help convert odorous ammonia to beneficial nitrates, and microbiome-friendly cleansing products. All green vegetables are low in carbohydrates and should became your basic daily nourishment.
Instead of this it shows which fruits and natural products known as healthy are not suitable for people suffering from high blood sugar and hiperinsulinemia. Our recipes have been gathered from around the world on our travels and others created by us and our supporting family.
I was age 30 at the time and had just moved to a new part of the UK and enlisted with a new doctors surgery.
I regularly go to the gym and run 10k and half marathon races, so the tiredness was noticeable. Through them, I noticed that some people were successfully curing hypothyroidism through the Paleo diet. He kindly responded very quickly saying, “I would say Paleo may be a bit dangerous, ideally I encourage you to follow a diet closer to this one.” He linked to the Perfect Health Diet. I asked him why he thought I had hypothyroidism, and whether he would recommend that I change my diet to help overcome it.
I was never over weight but I dropped a jean size, started noticing stomach muscles and people were commenting on me losing weight in my face. At this point the doctor had no comment except to say that I should stay at 50 mcg of levothyroxine daily. I continued to take 50 mcg levothyroxine daily, though in retrospect this would have been a good time to begin dropping the dose.
Although everyone has antibodies that can react to Neu5gc, the “preimmune repertoire” of antibodies binds to Neu5gc with very low affinity, and “low concentrations of anti-Neu5Gc antibodies do not seem to have any effect on Neu5Gc containing cells.” [4] In order to make high affinity antibodies, B cells must be repeatedly stimulated by Neu5gc-containing antigens. Gram-negative bacteria universally produce endotoxins that have been shown to be powerful immune system modulators through the Toll-like receptor 4 (TLR4) on a variety of human immune cells. There has been little study of the possibility that gut pathogens will incorporate Neu5Gc from food into their cell walls, potentially triggering autoimmunity against Neu5Gc incorporated in human cells. It looks like if you can generate large numbers of anti-Neu5Gc antibodies, then you are almost certain to get Hashimoto’s hypothyroidism. The 52.1% of hypothyroid patients who didn’t have Hashimoto’s generally had low levels of anti-Neu5Gc antibodies, similar to the healthy controls. The mimicry of human glycolipids and glycosphingolipids by the lipooligosaccharides of pathogenic neisseria and haemophilus.
Two of our most popular posts were about this problem: Low Carb Paleo, and LDL is Soaring – Help! It went down (to 378 8 months or so ago, time to check again) when I started supplementing with iodine. His talk at the Ancestral Health Symposium was on this topic, and a recent blog post, “The Central Role of Thyroid Hormone in Governing LDL Receptor Activity and the Risk of Heart Disease,” provides an overview.
T3 thyroid hormone binds to thyroid hormone receptors on the nuclear membrane, the pair (a “dimer”) is then imported into the nucleus where it acts as a transcription factor causing, among other effects, LDL receptors to be generated on the cell membrane.
So high T3 tends to reduce serum LDL cholesterol levels, but give cells more energy-providing fats. See Blood Lipids and Infectious Disease, Part I, Jun 21, 2011; Blood Lipids and Infectious Disease, Part II, Jul 12, 2011. Thyroid levels alter to encourage resource utilization when resources are abundant and to conserve resources when they are scarce. Apparently evolution favors immunity, and gives up the lipid-transport functions of LDL in order to maintain immune functions during periods of food scarcity. But if there is no infection and no toxins to oxidize LDL, and the diet creates no oxidative stress (ie low levels of omega-6 fats and fructose), then LDL particles may stay in the blood for long periods of time.
Eat more carbs, and address any remaining cause of hypothyroidism, such as iodine or selenium deficiency. And these infections may not oxidize LDL, thus they may not lead to loss of LDL particles by immune pathways. Blood pressure, blood sugar and blood lipids, it is claimed, will all come down on a low carb diet, in addition to weight. By July my total cholesterol was 350, LDL 280, and triglycerides bobbed around between 150 and 220. Jenny Ruhl has argued that within a period of months the situation should settle down and lipids should normalize. However, I doubted that an increase in saturated fat, or purging of visceral fat, would be responsible for a 75% increase in TC from 200 to 350.
If the surge was not entirely attributable to saturated fat, perhaps the better explanation was that the cholesterol was not being cleared properly. It has been claimed that excessively high or low cortisol, sustained over long periods, may cause one to get “stuck” in hibernation mode. Your T4 level will drop below range and you will be dependent on T3 until you wean yourself off. I would add: Increase the carbs if you find your free T3 falling to the bottom of the range. The rapid restoration of normal cholesterol levels with T3 supplementation would seem to prove that low T3 caused the high LDL levels.
It takes medical researchers years – often decades – to track down the causes of simple phenomena, such as high LDL on low carb.


Briefly, an extreme low-carb diet can create a glucose deficiency, especially if endurance exercise or infection increases glucose requirements, and glucose deficiency invokes the body’s glucose conservation measures, which primarily consist of lower T3 and higher rT3 hormone levels – two hormonal markers of euthyroid sick syndrome. Our thyroid expert, Mario Renato Iwakura, has been looking into Anthony’s papers to see if they report any negative effects from Perfect Health Diet-level carb intakes. Anthony seems to have supposed that my post was intended to reply or refute his July 1 post.
Hashimoto’s is a complex disease, whose causes are too complex to explore in this post, but in my opinion it is generally caused by exogenous toxins (gluten, mercury, bisphenol-A, bromide, etc) that disrupt gut flora and cause gut permeability and disturbed immunity that allows infections to enter the body and take root in thyroid tissue, after which in susceptible persons an autoimmune attack on the thyroid can develop. It is therefore necessary to look closely at each condition and at the literature to see which diet optimizes thyroid health – and whether specific thyroid disorders demand different diets.
100 g chicken breast supplies 165 calories total, 32 calories from fat and 133 from protein. It does not speak at all to Perfect Health Diet-style low carb (400 calories from starches, adequate protein) being unhealthy.
This catabolic reaction to carbohydrate deprivation is associated with decreased insulin secretion. On a 2483 calorie diet, this is only 420 carb+protein calories – insufficient to meet the minimum Paul estimated of 600-800 calories per day to avoid a glucose deficiency.
The Volek study [3] provided 8% carbs (184 calories) and 30% protein (704 calories) – still low-carb, but now enough carb and protein to avert a glucose deficiency. Just one wee problem: Volek et al didn’t even measure levels of T3, the critical thyroid hormone in question!
So it is no surprise that these zero-carb diets produce the elevated rT3 – depressed T3 pattern that is the body’s response to a glucose deficiency.
It looks like even high-carb diets can induce high rT3 and low T3 if the diet is unbalanced and deficient in protein. High rT3 and low T3 reduce metabolism and may help conserve protein during malnourishment, regardless of whether the threat to protein stores comes from dietary restriction of carbs or protein.
Subjects receiving the no-carbohydrate hypocaloric diets for two weeks demonstrated a similar 47% decline in serum T3 but there was no significant change in rT3 with time. Paul estimates that 200 calories of dietary carbs, plus 400 calories from gluconeogenesis, is barely sufficient to prevent a glucose deficiency in a sedentary healthy person.
So Spaulding et al is a positive contribution to the debate, and once again it tends to confirm Perfect Health Diet’s analysis. Both diets caused significant reductions in T3, with the ketogenic diet causing the largest decline. Paul himself discussed this study in last week’s post, in response to a cite by Danny Roddy. Effect of carbohydrate and noncarbohydrate sources of calories on plasma 3,5,3?-triiodothyronine concentrations in man.
The condition was discovered by accident when a nurse at the new surgery noticed I had an irregular heart beat. As I intermittently fasted in the mornings, my clarity of thinking improved at work in the mornings with reduced brain fog. I’m eagerly looking forward to my next blood test in three months to see if I am back to normal.
Cells need to be coated in these acids, because in water acids become ions and give the cells a charge, which repels other cells. Lipoproteins on Gram-positive and Gram-negative cell surfaces can also interact with TLR2, resulting in release of cytokines involved in B cell and T cell proliferation. Presumably free sialic acid is made available to such pathogens by other, sialidase-expressing bacteria living in the same niche, or … by host sialidases that are activated in the course of inflammation. Patients with hypothyroidism, some of whom have Hashimoto’s and some don’t, have an intermediate level of anti-Neu5Gc antibodies.
This observation strengthens the association between anti-Neu5Gc antibodies and autoimmune hypothyroidism.
This contact causes the LDL lipoprotein to be oxidized, after which the particle attaches to macrophage scavenger receptors and is cleared by immune cells.
Suboptimal thyroid might be the proximate cause for lipids rising on a low carb or paleo diet.
If stress is prolonged a condition called reverse T3 dominance occurs and lasts even after the stress passes and cortisol levels fall. I couldn’t find any studies confirming this claim, and don’t believe it is relevant to my case. I also offered my view, unchanged from our book, on what level of dietary carbohydrate intake is needed to avoid a glucose deficiency. In his first post (Low Carb High Fat Diets and the Thyroid, Aug 18, 2011), he showed that studies cited in Anthony’s July 1 post were generally very high omega-6 diets and therefore did not refute our diet, which prescribes low omega-6 intake. It was not; my post was intended as a treatment of thyroid health generally, and was designed to answer the question of whether the studies Anthony had cited in any way refuted the Perfect Health Diet prescription for thyroid patients. Slower but similar changes in the concentrations of T3 and rT3 to those of fasting occurred with administration of a protein-supplemented modified fast for 1 wk. The body simply isn’t being given enough amino acids to meet the body’s glucose requirements.
Instead, as I explained in my article, the pro-low-carb and Atkins-sponsored Volek team chose to only measure T3 uptake, a test also known as “resin-binding T3 uptake”. However, you cannot reasonably argue that T3 may have decreased with no detectable effect on the human body. The two diets that caused the greatest changes in T3 and rT3 were the first two: a diet of 100% fat and another of 50% fat and 50% protein.
In contrast, the same subjects receiving isocaloric diets containing at least 50 g of carbohydrate showed no significant changes in either T3 or rT3 concentration. They totally ignore all the other studies showing T3 reductions at higher carbohydrate intakes.
Any perturbation – exercise, infection, protein restriction limiting the availability of substrates for gluconeogenesis – might induce a glucose deficiency.
As carb+protein intake was insufficient to maintain glucose status, it is no surprise that the diets induced a fall in T3.
The remaining two diets were either low- or high-carbohydrate, and were consumed by all the subjects in random order between the two standard diet phases.
Paul’s observation was that high T3 levels are harmful to health, and that T3 may be elevated on the 80% carb diet in order to dispose of excess glucose (T3 stimulates glycolysis), so this could indicate a mechanism by which high-carb diets are health impairing. I was sent for blood tests in April 2012 where it was discovered that I had an underactive thyroid. He said my hypothyroidism “could be genetic” and “unfortunately it’s just who you are.” He also said that he wouldn’t recommend any dietary changes because I didn’t show symptoms of food intolerance. Other benefits included easier breathing through my nose, reduced tiredness in the day, and no more heart palpitations. I politely declined as I knew the diet was working and that there would be even better results to come.
When sialic acids are bound by antibodies, the charge is lost, and cells clump or aggregate. But Neu5gc from food doesn’t reach bone marrow, so there is nothing to stop the formation of white blood cells capable of generating antibodies to Neu5gc. In addition, bacterial DNA has been known for many years to have the capability to stimulate the immune system. This prevents LDL from serving its fat transport function, but keeps the LDL particles in the blood where their immune function operates.
But there is a significant minority of people on Paleo and other low carb diets whose blood lipids defy this claim.
Val recommends low carb for diabetics to prevent cholesterol and rT3 issues but warns not to go under 60g carb per day.
A 24-hour saliva test will give you an idea whether your cortisol levels are likely to contribute to an rT3 issue.
Anthony’s August 20 rebuttal cited a few more experiments which were not high in omega-6, and today Mario is going to look specifically at the issue of carbs. Urinary nitrogen excretion is a long-standing and widely employed marker for protein (as in, lean tissue) breakdown. You absolutely cannot say that T3 can decrease with no effect on testosterone, IGF-1, glucagon, sex hormone-binding globulin (SHBG), fat mass, or lean body mass. The first few weeks were a little tough as my body was becoming fat adapted but that soon passed.
In fact, clumping of cells after pig serum was injected into humans was the first sign that humans form antibodies to pig cells. It might also be a good idea to avoid very low carb if you are suffering from stress – such as lipid anxiety! How much carbohydrate intake is needed to avert a glucose deficiency as indicated by decreased T3 and increased rT3? Again, Perfect Health Diet recommends 400 calories (100g) carbohydrate, and argues that, because the amount of glucose that can be manufactured from protein is hormonally limited, even if dietary protein is sufficient at least 200 readily digestible glucose calories should be eaten to avert the risk of a glucose deficiency. Low-carb diets have repeatedly been shown to increase nitrogen excretion, which is one reason why they suck the big one for building muscle.
The diet left me feeling satiated the vast majority of the time and the food I was having were truly delicious combinations.



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