Applying Peat Principles To Veganism: Incredible Results

[Ritchie]

I remember last time I read it, this is a particularly interesting thread. @Ritchie are you still on this way of eating.
I recently found myself again needing to reintroduce starch. Also been frustrated because I've become fluffier since peating. Gained muscle too, but also fat around midsection and chest area. And I don't seem to be getting leaner.
Also on a no-starch way of eating I could not go more than 2-3 hrs without eating and would get hypoglycemia, especially when using thyroid.

Doubling down on carbs & restricting fats is the plan now.

I've reintroduced dairy and some gelatinous cuts of meat again. However, I think there is alot to be said for a plant based peaty style of eating. The changes the re-introduction of animal products have made don't seem significant and I still hold onto alot of the principles I was using when applying the Peat principles to veganism. I have never really cut oysters out mind you.

IMO the anti starch camp are misguided. Not all starches are created equal for starters, and in my experience potatoes and rice are irreplaceable staples. Not just within the window that you eat them but systemically overall as part of a consistent diet. They are invaluable to what I perceive to be consistent energy and blood sugar levels, sleep, like you mention not needing to constantly eat to feel ok, and hence consistent thyroid support, lowering cortisol, and generally a well functioning metabolic system. I love training as well, and starch definitely supports that. I've tried going extended periods without starch and everything seems to just work way better when they are included.

I also eat alot of fruit/juice and some sugar (not excessive amounts as the sugar defintiely seems to contribute to the fluff as you call it). Carrot salads are fantastic, and they have the only oil I add to my diet (coconut/olive). I don't hold excessive fat, mid section is lean, muscles strong and full. Training is great, recovery is great.

 

[Apple]

I've reintroduced dairy and some gelatinous cuts of meat again. However, I think there is alot to be said for a plant based peaty style of eating. The changes the re-introduction of animal products have made don't seem significant and I still hold onto alot of the principles I was using when applying the Peat principles to veganism. I have never really cut oysters out mind you.

IMO the anti starch camp are misguided. Not all starches are created equal for starters, and in my experience potatoes and rice are irreplaceable staples. Not just within the window that you eat them but systemically overall as part of a consistent diet. They are invaluable to what I perceive to be consistent energy and blood sugar levels, sleep, like you mention not needing to constantly eat to feel ok, and hence consistent thyroid support, lowering cortisol, and generally a well functioning metabolic system. I love training as well, and starch definitely supports that. I've tried going extended periods without starch and everything seems to just work way better when they are included.

I also eat alot of fruit/juice and some sugar (not excessive amounts as the sugar defintiely seems to contribute to the fluff as you call it). Carrot salads are fantastic, and they have the only oil I add to my diet (coconut/olive). I don't hold excessive fat, mid section is lean, muscles strong and full. Training is great, recovery is great.

Curious, How is your Hairline/Quality/Density ?
Eyesight/ do you wear glasses?

 

[Ritchie]

Curious, How is your Hairline/Quality/Density ?
Eyesight/ do you wear glasses?

I shave my hair, it's thin-ish at the hairline and looks way better shaved. Both Dad and grandparents are the same so I put it down to the blood line. My brother is the same as well.

Eyesight is 20/20, no glasses.

 

[Hugh Johnson]

Around 25, when people start looking "washed up" from american diets. Essentially the kidney are running low on bicarbonate. Then the skeleton is used as buffer to acid from protein, working out, alchol..etc. and the excess calcium release enters the soft tissue.

"Even in health, the physiological aging process causes a reduction of the renal function which begins at the age of 25 to 30. Thus acidosis, due to a deficit of bicarbonate, begins to develop early in life as a “normal” fate. The age-dependent renal function-loss can be precisely calculated with the “Cockcroft-formula”. At the age of 60 to 70 years the “normal” renal function will be reduced to about 50 % of the function at the age 25."

Are you sure it's bicarb deficiency, and not just alkaline deficiency? Because the rationale sounds a lot like part of Peat's rationale for eating lots of calcium, which is alkaline.

 

[Apple]

I shave my hair, it's thin-ish at the hairline and looks way better shaved. Both Dad and grandparents are the same so I put it down to the blood line. My brother is the same as well.

Eyesight is 20/20, no glasses.

Whould you share what your diet is like please ?
I think it is awesome that we have vegan alternative (RP friendly)

 

[GreekDemiGod]

I've reintroduced dairy and some gelatinous cuts of meat again. However, I think there is alot to be said for a plant based peaty style of eating. The changes the re-introduction of animal products have made don't seem significant and I still hold onto alot of the principles I was using when applying the Peat principles to veganism. I have never really cut oysters out mind you.

IMO the anti starch camp are misguided. Not all starches are created equal for starters, and in my experience potatoes and rice are irreplaceable staples. Not just within the window that you eat them but systemically overall as part of a consistent diet. They are invaluable to what I perceive to be consistent energy and blood sugar levels, sleep, like you mention not needing to constantly eat to feel ok, and hence consistent thyroid support, lowering cortisol, and generally a well functioning metabolic system. I love training as well, and starch definitely supports that. I've tried going extended periods without starch and everything seems to just work way better when they are included.

I also eat alot of fruit/juice and some sugar (not excessive amounts as the sugar defintiely seems to contribute to the fluff as you call it). Carrot salads are fantastic, and they have the only oil I add to my diet (coconut/olive). I don't hold excessive fat, mid section is lean, muscles strong and full. Training is great, recovery is great.

Thanks.
If you don’t mind asking, what was the reasoning of re-introducing dairy and meat?
Was it for the cravings/ taste, extra protein, perhaps Calcium?
Or it was a play-it-safe decision to ensure no long-term nutrient deficiencies develop.

And are you still Low Fat?

 

[Deleted member 5487]

Are you sure it's bicarb deficiency, and not just alkaline deficiency? Because the rationale sounds a lot like part of Peat's rationale for eating lots of calcium, which is alkaline.

Yeah Alkalinity salt like pot, mag, calcium.

But also are bicarbonate Precursors from breakdown of fruits/veggies.
Here is my masterlist on Acid-Base balance. Reading this connects to many dots, it crazy.

I currently enjoy a diet of Tubers, Root vegtables, Fruits and some protein/fat.

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"In the summaries, there is a wealth of data to show that metabolic acidosis has deleterious effects, particularly in patients with chronic kidney disease. A variety of hormonal abnormalities can occur, including insulin resistance, suppression of the growth hormone/IGF-1 axis, and increased circulating levels of glucocorticoids. Vitamin D production is suppressed and parathyroid hormone's sensitivity to calcium is reduced. In the absence of appropriate therapy, skeletal growth is impaired, muscle protein is subject to increased catabolism, and amino acids undergo increased oxidation: negative nitrogen balance results, and muscle wasting occurs. Ultimately, appropriate correction of metabolic acidosis with alkali can do much to ameliorate and correct this condition."


"not only kidney disease patients, but all individuals, have to be concerned about metabolic acidosis"

"Besides its direct effect on bone metabolism, metabolic acidosis can alter parathyroid hormone's sensitivity to ionized calcium. Graham and colleagues9 studied 8 hemodialysis patients with secondary hyperparathyroidism. They found that correction of metabolic acidosis increased the sensitivity of the parathyroid gland to ionized calcium, resulting in its suppression. Calcitriol did not have the same effect; however, rapid correction of metabolic acidosis in patients with renal failure resulted in a 2-fold response: circulating intact parathyroid hormone levels were suppressed, and vitamin D3 levels increased significantly10."

"Insulin resistance has been reported in patients with moderate to severe uremia. Fasting glucose levels tend to be elevated despite higher circulating levels of insulin, and there is an abnormal response to a glucose load. As a result, these patients have reduced sensitivity to the hypoglycemic action of insulin; defects in insulin secretion have also been reported11. As a complication of uremia, metabolic acidosis has been reported to contribute to insulin resistance. In rat studies, correction of metabolic acidosis partially corrects insulin resistance12. In patients not yet on dialysis, correction of metabolic acidosis with sodium bicarbonate has been shown to increase insulin sensitivity13. Mak14 studied 8 patients on chronic hemodialysis before and after 2 weeks of oral sodium bicarbonate therapy to correct the metabolic acidosis, and measured insulin sensitivity using the hyperinsulinemic euglycemic clamp technique. He also measured insulin secretion by the hyperglycemic clamp technique. Seven healthy volunteers served as control subjects. To control for the effect of the additional sodium, the patients and controls were also studied after 2 weeks of sodium chloride. Mak found that sodium bicarbonate therapy led to significant increases in venous pH and serum bicarbonate levels. There was no significant change in parathyroid hormone concentrations; however, circulating 1,25 dihydroxyvitamin D3 levels, which had been low prior to treatment with sodium bicarbonate, increased significantly following treatment. Insulin sensitivity and secretion increased as well following sodium bicarbonate therapy. Sodium chloride had no effect."

"Still other hormones are affected by metabolic acidosis. In normal adults, metabolic acidosis lowers serum levels of free triiodothyronine (T3) and thyroxine (T4), and thyroid-stimulating hormone (TSH) levels are mildly increased. The concentration of reverse T3 is unchanged. The clinical significance of this mild hypothyroid state is unknown, but it could affect both calcium and protein metabolism."

"It has long been noted that patients with chronic kidney disease appear malnourished. In the early 17th century, physicians from France and England who visited St. Petersburg to attend Peter the Great noted how emaciated he appeared. They concluded that his appearance was due largely to the sequella of his disease. About 300 years later, Lyon, Dunlop, and Stewart17 advocated the use of alkali for the treatment of patients with kidney disease. They noted a connection between renal failure and metabolic acidosis, and attributed the latter as a cause of malnutrition in this disease. As did others, they noted that a low protein diet was beneficial for treatment of patients with kidney disease. Giordano18 would later verify through detailed dietary records that there was a relationship between a reduction in protein intake and relief of uremic symptoms. Today we know that protein, particularly animal protein, is rich in sulfur-containing amino acids and is a major source of acid in the diet. It is this acidosis that has a negative impact on the body's protein stores. Coles19, who performed careful measurements of various muscle groups in patients with chronic kidney disease, demonstrated that a decrease in muscle mass was often masked by fluid retention. He concluded that patients with kidney disease were malnourished."

"How does metabolic acidosis cause protein wasting? It would seem intuitively obvious that metabolic acidosis would act directly on cells and lower intracellular pH, but the available evidence suggests that this is not the case. When metabolic acidosis is induced in rats by feeding them ammonium chloride in the diet or by infusing them with hydrochloric acid, or by induction of chronic renal failure, intracellular pH as measured by 31 PNMR (phosphorus nuclear magnetic resonance) is maintained despite the severity of the low extracellular pH21. [!!] This work suggests that other signal transduction pathways must be involved when metabolic acidosis stimulates muscle proteolysis. A prime mediator of this process appears to be glucocorticoids. When May and colleagues22 induced chronic renal failure in rats, they noted that urinary corticosterone levels increased in proportion to the degree of metabolic acidosis. Moreover, they found that only the acidotic rats had accelerated rates of muscle protein degradation. When sufficient sodium bicarbonate was added to the diet to correct the acidosis, urinary corticosterone levels remained elevated but rates of protein degradation were no different from those in control rats. The authors concluded that both acidosis and a high glucocorticoid level were required to stimulate muscle proteolysis. Garibatto and colleagues23 extended these results to patients with chronic kidney disease. They also found an inverse correlation between serum cortisol and bicarbonate levels—ie, the lower the serum bicarbonate levels, the higher the serum cortisol levels. They also measured rates of protein degradation in these patients and found that higher rates of protein degradation correlated directly with serum cortisol levels and indirectly with serum bicarbonate levels. Although a correlation between serum cortisol levels and serum bicarbonate levels exists in the setting of metabolic acidosis, it does not prove causality. More definitive evidence for this cause-and-effect relationship comes from both cell culture work and animal studies."

"Glucocorticoids alone did not stimulate protein degradation. Only in the presence of both glucocorticoids and acidosis could protein degradation occur."
It's almost a sign of things going down of the hills.

"Besides an increase in protein degradation, metabolic acidosis is accompanied by an acceleration of amino acid oxidation. Because they play an important role in protein metabolism, the branched-chain amino acids have served as markers of malnutrition in various disease states, including chronic kidney disease. The branched-chain amino acids include valine, leucine, and isoleucine and constitute 18% of the amino acids in muscle. Altered cellular and serum levels of the branched-chain amino acids are regularly found in patients with chronic kidney disease31, and the relative abundance reflects disease severity."

"even short-term correction of metabolic acidosis has implications for patients with chronic kidney disease. Even patients with fairly advanced chronic kidney disease can potentially benefit from correction of metabolic acidosis."


- Diet-Induced Low-Grade Metabolic Acidosis and Clinical Outcomes: A Review

"Diet-induced low-grade metabolic acidosis is a condition that has been investigated since the early 1980s, when Kurtz et al. (1983) [4] showed that an increased dietary acid load led to small changes in the acid-base balance (increase in [H+] and reduction in [HCO3−]). From time to time, other studies have been published focusing on these minimal alterations in the acid-base balance [5,6,7,8], and several terminologies have been used, such as "eubicarbonatemic metabolic acidosis" [9] and "acid retention" [10]."

"The nutrients that release acid precursors into the bloodstream are phosphorus and proteins (mostly containing sulfur amino acids, such as cysteine, methionine, and taurine, and cationic amino acids such as lysine and arginine). In addition, sodium chloride (NaCl) intake is reported to be an independent predictor of plasma bicarbonate concentration. Assuming a causal relationship, NaCl may exert approximately 50–100% of the acidosis-producing effect of the dietary acidic load, and is therefore considered a predictor of diet-induced low-grade metabolic acidosis [14]. On the other hand, the nutrients that are precursors of bases are potassium, magnesium, and calcium. Thus, in general, the main foods that release precursors of acids into the bloodstream are mostly of animal origin (except for beans and nuts), and foods that are precursors of bases are mainly those of plant origin [2,3]."

"the foods that contribute most to the release of acids into the bloodstream are meats (beef, pork, or poultry), eggs, beans, and oilseeds, and the foods that contribute most to the release of bases are fruits and vegetables. If there is an excessive consumption of acid precursor foods, to the detriment of those precursors of bases, volubility of the acid-base balance occurs [2,3,17]. If this acid-base balance disorder occurs in a prolonged and chronic way, low-grade metabolic acidosis may become significant and predispose to diseases [18,19,20,21]."

"Some mechanisms have been proposed to explain the influence of an increased dietary acid load on bone metabolism (Figure 2). The slight reduction of the extracellular fluid pH suppresses the activity of osteoblasts and decreases the gene expression of specific matrix proteins and alkaline phosphatase activity. In addition, low-grade metabolic acidosis has been associated with osteoclast activity and increased urinary calcium excretion without increased intestinal calcium absorption, resulting in the depletion of bone calcium [22,23]. Net acid excretion (NAE), a predictor of the acidifying potential of the diet, is shown to be associated with increased serum levels of parathyroid hormone (PTH) and the urinary excretion of calcium and N-telopeptide, an important marker of bone resorption [20]. In the study conducted by Buclin et al. (2001) [11], the ingestion of an acidogenic diet for four days caused an increase in the urinary excretion of calcium and C-telopeptide of 74% and 19%, respectively, compared to the intake of an alkalizing diet for the same period. Moreover, the consumption of this dietary pattern was associated with a discrete, but significant, reduction in blood and urinary pH."

"Studies have shown that the deleterious effects of low-grade metabolic acidosis on bone tissue are independent of calcium intake [11,27]."
"Recently, Kong et al. (2017) [28] showed in their study with 7187 participants from the Korean National Health and Nutrition Examination Survey (KNHANES) that the dietary intake of potassium was positively associated with a higher mineral density in the lumbar spine, femur, and hip, even in participants with a low dietary calcium intake—a fact that can be attributed to the lower acidifying potential of diets rich in food sources of potassium [28]."

"[..]dietary proteins (mainly animal sources) may exert an anabolic effect on bone turnover by increasing levels of insulin-like growth factor (IGF-1), stimulating intestinal calcium absorption, suppressing PTH action, and improving shape and muscle mass [32,33,34]. Furthermore, bones are formed by the protein matrix, and dietary proteins appear to exert an osteotrophic effect [33,35]. Considering these facts together, it is raised that in the presence of an adequate dietary intake of base-forming nutrients, proteins may exert benefits on the bones [32]."

"The effects of an acidogenic diet on the formation of kidney stones are the clinical outcome with the highest number of published studies. In response to diet-induced low-grade metabolic acidosis, the kidneys perform adaptive responses in an attempt to restore the acid-base balance, and these responses include an increased excretion of calcium and oxalate salts, and reduced citrate excretion. Citrate inhibits the formation and agglomeration of calcium oxalate crystals and, thus, the reduction of its excretion is associated with the formation of a less soluble complex of calcium oxalate [2,36]."

"Two mechanisms have been proposed to elucidate the associations between dietary acid load and chronic kidney disease (CKD). As the demand for acid elimination rises, there is an increase in endothelin-1, angiotensin II, and aldosterone production. These substances are associated with the reduction of the glomerular filtration rate (GFR) and the stimulation of pro-fibrotic factors, which are associated with renal fibrosis. In addition, in an attempt to neutralize the H+ load, an increase in ammonia production occurs in the proximal tubule, which can cause tubular toxicity and renal damage. These processes, when constantly stimulated, are associated with the increased risk and progression of CKD [39,40,41]."

"In this context, it has been shown that the serum bicarbonate level is an independent predictor of CKD progression. Raphael et al. (2011) [42] showed that higher serum bicarbonate levels within the normal range (20 to 30 mEq/L) are associated with a reduced risk of negative outcomes in patients with CKD, as dialysis, worsening renal function, and death [42]."

"In the summaries, based on available data, the dietary acid load seems to be an important predictor of CKD and interventions taking into account the frequent consumption of base-producing foods, such fruit and vegetables, should be considered."

"The mechanism involving the association between dietary acid load and the risk of diabetes mellitus has not yet been fully elucidated, but it is believed that the maintenance of blood pH close to the lower limit of the normal range may lead to a decrease in the uptake of glucose by the muscle, the disruption of insulin binding to its receptor, and the inhibition of the insulin signaling pathway. This may lead to peripheral insulin resistance, the main risk factor for the development of type 2 diabetes mellitus [22]."

"Some mechanisms are suggested to justify the association between a high acid diet load and the risk of hypertension. In the presence of low-grade metabolic acidosis, there is an increase in the pituitary stimulus for ACTH synthesis and a consequent production of cortisol and aldosterone [56], which in excess, may induce an increase in blood pressure [57,58]. In addition, the acid-base balance influences mineral homeostasis by regulating the calcium absorption in the kidneys, and it is reported that the increased urinary excretion of this mineral may be associated with an increased blood pressure [59,60]. In addition, NaCl intake, the most known risk factor associated with the etiology of hypertension, is an independent predictor of diet-induced low-grade metabolic acidosis [14]."

"Recently, Chan et al. (2015) [61] evidenced a positive association between the acidogenic diet and the risk of non-alcoholic hepatic steatosis (NASH) in 793 Chinese individuals aged 19–72 years. An increase of 1.32 in the odds of developing NASH, independently of the intake of fiber, saturated fatty acids, carbohydrates, and proteins—dietary constituents known to influence the risk of NASH–was observed for each 20 mEq/day of NEAP [61]. Although this is the only available study evaluating this association, it can be suggested that the influence of diet on the acid-base balance is a factor that contributes to the development of this disease.

The mechanisms by which an acidogenic diet may influence the pathogenesis of NASH are not fully understood. Taking into account that the slight reduction in plasma pH caused by an acidifying diet is associated with insulin resistance, the consequent hyperglycemia and increased inflammation could contribute to hepatic insulin resistance, which is related to the increase in the availability of free fatty acids, and is a risk factor for the development of the disease [62]."

"The mechanism that surrounds the association between a high dietary acid load and the loss of muscle mass involves the effect of low-grade metabolic acidosis on the stimulation of the proteolysis pathways. This stimulus can be triggered by an increased production of glucocorticoids, such as cortisol, which stimulates the degradation of amino acids for release into the bloodstream. Glutamine is essential for the process of tubular ammoniagenesis, important for the elimination of the body’s hydrogen ions [66,67]."

"Studies have shown that diets with high values of NEAP and PRAL may predispose to several metabolic damages, such as the stimulation of bone resorption associated with a decrease in bone mineral density and bone mass, leading to a higher risk of fractures. There are some interventional and observational studies showing that increasing fruit and vegetable consumption is associated with better bone outcomes, such as reduced reabsorption markers excretion, an increased bone mineral content, and lower fractures and osteoporosis risk [27,71,72,73]. Furthermore, other studies have reported that alkalinizing supplementation (including potassium citrate or potassium bicarbonate) can attenuate the deleteriuous effects of low-grade metabolic acidosis on bone tissue, as demonstrated by Dawson-Hughes et al. (2009 and 2015) [74,75] and Moseley et al. (2013) [76]. However, the effects promoted by alkalinizing supplementation are acute and there must be a dietary pattern change to reduce the risk of negative bone outcomes, and the frequent consumption of base-producing foods should be considered."

"Some studies have shown that a slight reduction in extracellular pH decreases the beta cell response and leads to a disruption of insulin binding to its receptor. This may lead to peripheral insulin resistance, the main risk factor for the development of type 2 diabetes mellitus [78,79,80]. In addition to high PRAL and NEAP values, other markers of metabolic acidosis have been associated with insulin resistance, such as plasma bicarbonate reduction, an increased anion gap, elevated levels of plasma lactate, and low urinary pH values [12,51,52,80]."

"[..]it has been suggested that intracellular potassium reduction is compensated for by elevated sodium levels and, as a consequence, blood pressure elevation [87]. In this context, studies have showed that a higher intake of fruit, vegetables [88,89,90], and some specific nutrients (i.e., potassium and magnesium) [91,92,93] are associated with a lower hypertension risk. However, there are no studies evaluating the effect of specific dietary interventions correcting low-grade metabolic acidosis on the hypertension risk."


- Chronic Metabolic Acidosis Destroys Pancreas((

Travisord would probably add [sick!] after destroys.

I was quoting it but gave up halfvvay through because it's a painful text, quite confusing. On the hands of the others, the references are good and it's worth checking them out.

Ps.: found this version which had an intervention from a voice of reason.


- Diet-induced acidosis: is it real and clinically relevant?

"The normalisation of a low-grade chronic metabolic acidosis has been accomplished by two methods: change in dietary patterns and alkaline supplementation."

"Reducing protein consumption down to the US dietary recommended intake in a trial of thirty-nine healthy premenopausal women has also been shown to reduce Ca excretion and raise urinary pH, as well as reduce markers of bone resorption (48). It should be emphasised that this trial did not evaluate a low-protein diet, but rather lowered what could be considered a high protein intake to a level of 0·8 g/kg for this population. Because renal NH4+ formation is dependent upon adequate protein intake, an extremely protein-deficient diet may also increase acidosis (49). In fact, in a recent study of 161 postmenopausal women, protein intake had a positive association with lumbar bone mineral density, but only after adjusting for the negative effect of the sulfur content of the proteid (sulfate), perhaps ‘reconciling reports of positive impacts of dietary protein on bone health with reports of a negative impact of the acid load from sulfur-containing amino acids’ (50). In children, a greater protein intake has been associated with greater bone strength, though this effect is negated if alkalinising nutrients are lacking. It should be noted, however, that clearly bone may be influenced by these minerals in ways unrelated to acid–base chemistry (51)."

"Finallies, increasing sodium chloride intake dose-dependently decreases blood pH and plasma bicarbonate levels (52), independent of the partial pressure of carbon dioxide (PCO2), creatinine clearance and dietary acid load (6). This effect may be due to a decrease in the strong ion difference, as total chloride concentration increases relative to total N and a concentration, an effect that may increase H+ concentration (53). Subjects who are particularly sensitive to salt, generally defined as an increase of 3 to 5 mmHg for a given salt load, have more of a metabolic acidosis than those subjects who are salt resistant (54). So, while everyone’s net acid load would improve by lowering their dietary salt intake, some individuals should benefit more than others from this dietary intervention."

"A number of supplemental interventions have also been used. Salts of carbonic acid are available in a variety of formats. These include sodium or potassium bicarbonate and calcium carbonate. Alkali salts are also available as citrate, acetate or hydroxides. As suggested above, giving Na salts may be partly counterproductive, given their other effects, and so most studies use K or Ca alkali salts. These salts dose-dependently decrease NAE (55,56).
Caution using alkali therapy without careful consideration and expertise in subjects with heart, lung or kidney disease is needed. In congestive heart failure, sodium bicarbonate impairs arterial oxygenation and reduces systemic and myocardial oxygen consumption in these patients, which may lead to transient myocardial ischaemia (57). Additionally there may be several simultaneous processes affecting acid–base status among patients with congestive heart failure (58). Similarly, bicarbonate loading may worsen exercise response in chronic obstructive pulmonary disease patients (59). Finally, subjects with kidney failure may develop elevated blood K levels and potentially fatal cardiac arrhythmias if given K alkali salts, or volume overload and breathing problems if given Na alkali salts."

 

[Ritchie]

Thanks.
If you don’t mind asking, what was the reasoning of re-introducing dairy and meat?
Was it for the cravings/ taste, extra protein, perhaps Calcium?
Or it was a play-it-safe decision to ensure no long-term nutrient deficiencies develop.

And are you still Low Fat?

Yes it’s really a play it safe and cover all based type thing. Particularly because I live quite an active lifestyle. Dairy for calcium and gelatinous meat for the gelatin, also the ease of protein source from them.

Yep still relatively low fat. Any fat that I do have is saturated (coconut oil in carrot salads and the fat that is in the dairy and meat)

 

[looking2grow96]

Are you still vegan and going strong @Ritchie ?

 

[Ritchie]

Are you still vegan and going strong @Ritchie ?

Not vegan anymore but incorporate alot of the principles.
I eat some gelatinous cuts of meat here and there and dairy, mainly just to cover the bases because I train alot.. but tbh not sure if I need them. Was doing very well full plant based supplementing with some oysters and liver here and there, and I think if you are high carb/high sugar this way of eating is very synergistic for metabolism.

 

[LiveLaughLove]

Rice and potatoes both have very low tryptophan, methionine and cysteine levels. Haven't looked at the other starches..

Yeah I don't think it's good to be constantly taking T3 as a means to ramp up your metabolism. I think it could have a place in the beginning if you're metabolism is completely tanked, but to me it's a sign of there being a systemic issue if you have to keep taking it chronically.

Peat’s research includes such statements as “T3 stimulates new thyroid genesis. Progesterone stimulates new progesterone genesis.” This is why Ray advocates astronomically smaller doses than mainstream docs (4-15mcg of t3 over long term, vs the commonly dosed 40-60mcg).

 

[Ritchie]

Peat’s research includes such statements as “T3 stimulates new thyroid genesis. Progesterone stimulates new progesterone genesis.” This is why Ray advocates astronomically smaller doses than mainstream docs (4-15mcg of t3 over long term, vs the commonly dosed 40-60mcg).

I get the logic. It just doesn’t work that way in practice for me. Maybe a little bit supplemented here and there I think can be beneficial (perhaps every few days a couple of mcg t3), but not everyday.

 

[LiveLaughLove]

I get the logic. It just doesn’t work that way in practice for me. Maybe a little bit supplemented here and there I think can be beneficial (perhaps every few days a couple of mcg t3), but not everyday.

Word.

I found it a pleasant surprise that I needed to consume about twice as much of all macros without gaining weight while on t3. I encourage playing around with it more (albeit all the wisdom and knowledge of dosing via Danny and Ray).

I keep finding that much of Ray Peat’s most extensive work-backed suggestions that get some of the most underrated appreciation (supping thyroid/preg/hormones), when done in tandem with fixing the diet, yield manifold dividends compared to whatever someone’s version of “natural” leads them to dismiss a hormonal supp.

 

[GreekDemiGod]

What are the best vegan Calcium sources?

 

[RPDiciple]

Not vegan anymore but incorporate alot of the principles.
I eat some gelatinous cuts of meat here and there and dairy, mainly just to cover the bases because I train alot.. but tbh not sure if I need them. Was doing very well full plant based supplementing with some oysters and liver here and there, and I think if you are high carb/high sugar this way of eating is very synergistic for metabolism.

Im also training a lot with weights and building muscles. I have experimented with the 50g protein or a little more lately after ray talking about it. I have not noticed much really positive or negative. How much protein are you consuming? I was hoping to get warmer when i reduced it

 

[PeskyPeater]

good day

where do gorilla get there B12 from , termites and other insects? No, accidental eating of soil and their own feces containing B12.
Vegans, good luck with that.

 

[Xin]

Veganism initially gave me great results but 2 years into it, I was in worse condition than my peers who are pretty much anything. It's simply the worst diet when it comes to gut health, physical and mental performance.

 

[PeskyPeater]

The available evidence for caseins, both in their complete form and in fragments resulting from their enzymatic degradation, reveal an enhancement of different aspects of the immune system, but their potential as antitumour agents has been scarcely explored. The use of caseins or their peptides to enhance the immune system to fight cancer is a rational strategy, as the immune system constantly works to keep us free of tumours. However, it is, of course, not always successful, with an estimated 19,520 new cases of AML diagnosed in the United States in 2018, accounting for approximately one-third of all new leukaemia cases [115]. Nevertheless, enhancing the immune system to eradicate cancer remains a valid and widely explored strategy against cancer. There are elements that suggest that caseins or casein peptides could eradicate leukaemia by functioning as enhancers of the immune system and inducing cell death of malignant cells.

As we noted above, the mechanisms of the antileukaemic action of SC in vivo are unknown, but all these data on casomorphins, added to the fact that both granulocytes and macrophages are capable of hydrolysing caseins to release biologically active peptides [55, 56], suggest to us that these opioid peptides may be responsible for the antileukaemic effects observed for SC or caseins [116]

 

[PeskyPeater]

above is a reaction to:

From the Peat perspective, I can think of a few reasons as to why this is working so well:
..
6. No IGF-1 or casomorphins from the dairy.
..

 

[PeskyPeater]

From the Peat perspective, I can think of a few reasons as to why this is working so well:

8. Good quality protein from the legumes, potatoes, etc with very good amino acid profile.

as veganism is an elimination diet, and protein can be antimetabolic by decreasing the carb/protein ratio, and the storage form of protein of plant are of such low quality that this low protein diet improves the carb ratio upward. And this activates the mTOR pathway autophagy to repair cells in sleep. So without knowing it, vegans ar improving thyroid function and the carbs help to spare bodies protein, while repair is activated and this is antiaging, for a while at least