Try Grapefruit Juice

[Deleted member 5487]

Grape Fruit Juice has 37% more Potassium Citrate than Orange or Lemon juice. Making it much stronger at booster to overall alkalinity, As citrate is converted into carbon dioxide and then bicarbonate. I even add a tablespoon of sodium citrate to the carton to boost the citrate further. Grape fruit juice is much more tart due to citrates, but the sugar content is about the same.

Those that follower my alkalinity theory work should give it a try.

My base case is everyone over the age of 25 should be focusing intentionally on PRAL and alkalinity as the main component of the diet.

Just SO happens that peats protein source of Diary is about net nuteral on PRAL and orange juice has one of the highest citrate concentrations.


"

"Acid-base balance in the body influences adrenal hormone production of cortisol. When bicarbonate [HCO3- levels are low, the kidneys upregulate glutaminase activity and trigger cortisol production [35-37]." "Dietary induction of acidosis increases serum cortisol concentrations [38]."

"Cortisol activates the tryptophan metabolism pathway which is carried out by rate-limiting enzymes of tryptophan catabolism, 2,3-dioxygenase (TDO) and indoleamine 2,3-dioxygenase (IDO). Cortisol directly stimulates TDO activation and may augment IDO activity indirectly through inflammatory cytokine signaling such as interferon gamma [49,50]. Excessive or chronic cortisol production acquired from a ‘Western’ dietary lifestyle could play a role in augmenting the tryptophan metabolism pathway and drive downstream molecular events that promote carcinogenesis."

"Upregulated cortisol bioactivity driven by diet-induced acidosis may be a factor in metabolic syndrome by promoting insulin resistance. Chronic hyperglucocorticoidism upregulates visceral obesity while reducing insulin sensitivity mainly in visceral adipocytes which appear to be more responsive to cortisol than subcutaneous adipocytes due to higher expression levels of glucocorticoid receptors [58,59]."

"Acidosis associated insulin resistance through cortisol activity may result in compensatory pancreatic insulin secretion and higher levels of circulating insulin in the serum, a condition known as hyperinsulinemia." As Travisord would say: [sick]

"The Primary Sources Of Acidity In The Diet Are Sulfur-containing AAs, Salt, And Phosphoric Acid"

- Acidosis: An Old Idea Validated by New Research (the author appears to be credible, you can tell because he's wearing a tie and has his arms crossed) "The idea that “being too acid” contributes to disease susceptibility, especially cancer, has been around for a long time in the...

raypeatforum.com

"Most of us eat a diet that imposes a net acid load, so our kidneys tend to conserve citrate and α-Ketogluterate, our intercalated cells pump protons not bicarbonate in to the final urine, our proximal tubules produce considerable ammonia and our urine pH is about 5 – 6.

Some of us, vegetarians whose diets do not have a proper balance of protein, very massive fruit eaters, as examples, have low citrate reabsorptions and high distal deliveries of α-Ketogluterate; our intercalated cells are reversed and stimulated to put bicarbonate into the final urine, our proximal tubules do not make much ammonia.

But the words ‘most’ and ‘some’ are misleading. In the US, certainly, chronic acid loading is the overwhelming rule, and the same throughout Europe and considerable parts of urban Asia. So our ‘normal’ poise centers on adaptations to acid load. It is not that we live in a neutral acid base condition, demanding from our kidneys little excretion of acid or of alkali. Life long we demand acid excretion. That is where we start. It is to that task our kidneys – and our bones, as I shall someday speak about – apply themselves all the days of our lives. However it is, for good or for evil, that lifelong adaptation to acid load affects us, that is our state, our permanent condition."

HOW POTASSIUM CITRATE PILLS WORK | Kidney Stone Program

kidneystones.uchicago.edu

Quantitative analysis revealed the highest concentration of citrate was in grapefruit juice (64.7 mmol/L), followed in decreasing concentrations by lemon juice (47.66 mmol/L), orange juice (47.36 mmol/L), pineapple juice (41.57 mmol/L), reconstituted lemonade (38.65 mmol/L),

 

[ecstatichamster]

Dr. Peat has pointed out that grapefruit contains some ingredients that increase estrogen and jam up the liver's ability to detoxify, so I avoid all grapefruit products. There are many drugs that have side effects when taken with grapefruit, so I think this view is validated and I would never consume it.

Grapefruit, Flavonoids, Detoxification, and Estrogen – Functional Performance Systems (FPS)

For example, the flavonoids, naringenin, quercetin and kaempherol (kaempherol is an antioxidant, a phytoestrogen, and a mutagen) modify the metabolism of estradiol, causing increased bioavailability of both estrone and estradiol. (W. Schubert, et al., “Inhibition of 17-beta-estradiol metabolism by grapefruit juice in ovariectomized women,” Maturitas (Ireland) 30(2-3), 155-163, 1994.) -Ray Peat, PhD

 

[Deleted member 5487]

Dr. Peat has pointed out that grapefruit contains some ingredients that increase estrogen and jam up the liver's ability to detoxify, so I avoid all grapefruit products. There are many drugs that have side effects when taken with grapefruit, so I think this view is validated and I would never consume it.

Grapefruit, Flavonoids, Detoxification, and Estrogen – Functional Performance Systems (FPS)

For example, the flavonoids, naringenin, quercetin and kaempherol (kaempherol is an antioxidant, a phytoestrogen, and a mutagen) modify the metabolism of estradiol, causing increased bioavailability of both estrone and estradiol. (W. Schubert, et al., “Inhibition of 17-beta-estradiol metabolism by grapefruit juice in ovariectomized women,” Maturitas (Ireland) 30(2-3), 155-163, 1994.) -Ray Peat, PhD

Are those same flavonoids found orange juice and guava juice?

 

[mostlylurking]

Dr. Peat has pointed out that grapefruit contains some ingredients that increase estrogen and jam up the liver's ability to detoxify, so I avoid all grapefruit products. There are many drugs that have side effects when taken with grapefruit, so I think this view is validated and I would never consume it.

Grapefruit, Flavonoids, Detoxification, and Estrogen – Functional Performance Systems (FPS)

For example, the flavonoids, naringenin, quercetin and kaempherol (kaempherol is an antioxidant, a phytoestrogen, and a mutagen) modify the metabolism of estradiol, causing increased bioavailability of both estrone and estradiol. (W. Schubert, et al., “Inhibition of 17-beta-estradiol metabolism by grapefruit juice in ovariectomized women,” Maturitas (Ireland) 30(2-3), 155-163, 1994.) -Ray Peat, PhD

 

[Dave Clark]

Dr. Peat has pointed out that grapefruit contains some ingredients that increase estrogen and jam up the liver's ability to detoxify, so I avoid all grapefruit products. There are many drugs that have side effects when taken with grapefruit, so I think this view is validated and I would never consume it.

Grapefruit, Flavonoids, Detoxification, and Estrogen – Functional Performance Systems (FPS)

For example, the flavonoids, naringenin, quercetin and kaempherol (kaempherol is an antioxidant, a phytoestrogen, and a mutagen) modify the metabolism of estradiol, causing increased bioavailability of both estrone and estradiol. (W. Schubert, et al., “Inhibition of 17-beta-estradiol metabolism by grapefruit juice in ovariectomized women,” Maturitas (Ireland) 30(2-3), 155-163, 1994.) -Ray Peat, PhD

This is where Ray confuses me/people at times. Oranges, which he is big on, has naringenin, and probably some of the other flavanoids.

Effect of Citrus Flavonoids, Naringin and Naringenin, on Metabolic Syndrome and Their Mechanisms of Action

Flavonoids are important natural compounds with diverse biologic activities. Citrus flavonoids constitute an important series of flavonoids. Naringin and its aglycone naringenin belong to this series of flavonoids and were found to display strong anti-inflammatory ...

www.ncbi.nlm.nih.gov

 

[YourUniverse]

Grape Fruit Juice has 37% more Potassium Citrate than Orange or Lemon juice. Making it much stronger at booster to overall alkalinity, As citrate is converted into carbon dioxide and then bicarbonate. I even add a tablespoon of sodium citrate to the carton to boost the citrate further. Grape fruit juice is much more tart due to citrates, but the sugar content is about the same.

Those that follower my alkalinity theory work should give it a try.

My base case is everyone over the age of 25 should be focusing intentionally on PRAL and alkalinity as the main component of the diet.

Just SO happens that peats protein source of Diary is about net nuteral on PRAL and orange juice has one of the highest citrate concentrations.


"

"Acid-base balance in the body influences adrenal hormone production of cortisol. When bicarbonate [HCO3- levels are low, the kidneys upregulate glutaminase activity and trigger cortisol production [35-37]." "Dietary induction of acidosis increases serum cortisol concentrations [38]."

"Cortisol activates the tryptophan metabolism pathway which is carried out by rate-limiting enzymes of tryptophan catabolism, 2,3-dioxygenase (TDO) and indoleamine 2,3-dioxygenase (IDO). Cortisol directly stimulates TDO activation and may augment IDO activity indirectly through inflammatory cytokine signaling such as interferon gamma [49,50]. Excessive or chronic cortisol production acquired from a ‘Western’ dietary lifestyle could play a role in augmenting the tryptophan metabolism pathway and drive downstream molecular events that promote carcinogenesis."

"Upregulated cortisol bioactivity driven by diet-induced acidosis may be a factor in metabolic syndrome by promoting insulin resistance. Chronic hyperglucocorticoidism upregulates visceral obesity while reducing insulin sensitivity mainly in visceral adipocytes which appear to be more responsive to cortisol than subcutaneous adipocytes due to higher expression levels of glucocorticoid receptors [58,59]."

"Acidosis associated insulin resistance through cortisol activity may result in compensatory pancreatic insulin secretion and higher levels of circulating insulin in the serum, a condition known as hyperinsulinemia." As Travisord would say: [sick]

"The Primary Sources Of Acidity In The Diet Are Sulfur-containing AAs, Salt, And Phosphoric Acid"

- Acidosis: An Old Idea Validated by New Research (the author appears to be credible, you can tell because he's wearing a tie and has his arms crossed) "The idea that “being too acid” contributes to disease susceptibility, especially cancer, has been around for a long time in the...

raypeatforum.com

"Most of us eat a diet that imposes a net acid load, so our kidneys tend to conserve citrate and α-Ketogluterate, our intercalated cells pump protons not bicarbonate in to the final urine, our proximal tubules produce considerable ammonia and our urine pH is about 5 – 6.

Some of us, vegetarians whose diets do not have a proper balance of protein, very massive fruit eaters, as examples, have low citrate reabsorptions and high distal deliveries of α-Ketogluterate; our intercalated cells are reversed and stimulated to put bicarbonate into the final urine, our proximal tubules do not make much ammonia.

But the words ‘most’ and ‘some’ are misleading. In the US, certainly, chronic acid loading is the overwhelming rule, and the same throughout Europe and considerable parts of urban Asia. So our ‘normal’ poise centers on adaptations to acid load. It is not that we live in a neutral acid base condition, demanding from our kidneys little excretion of acid or of alkali. Life long we demand acid excretion. That is where we start. It is to that task our kidneys – and our bones, as I shall someday speak about – apply themselves all the days of our lives. However it is, for good or for evil, that lifelong adaptation to acid load affects us, that is our state, our permanent condition."

HOW POTASSIUM CITRATE PILLS WORK | Kidney Stone Program

kidneystones.uchicago.edu

Quantitative analysis revealed the highest concentration of citrate was in grapefruit juice (64.7 mmol/L), followed in decreasing concentrations by lemon juice (47.66 mmol/L), orange juice (47.36 mmol/L), pineapple juice (41.57 mmol/L), reconstituted lemonade (38.65 mmol/L),

Im excited to see how your theory keeps unfolding going forward. Have you continued to notice health improvements from its implimentation?

What are your thoughts on quinine? Apparently grapefruit contains chemicals very similarto quinine, which has been used as an anti-parasitic, serotonin-antagonist.

 

[Deleted member 5487]

Im excited to see how your theory keeps unfolding going forward. Have you continued to notice health improvements from its implimentation?

What are your thoughts on quinine? Apparently grapefruit contains chemicals very similarto quinine, which has been used as an anti-parasitic, serotonin-antagonist.

I am, I feel much better on grapefruit juice than orange juice.

Alkalinity has a direct effect on Thyroid.

""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.""


Here is the master list for those wanting a deep read. Mind blowing as it's all related. parathyroid, thyroid, cortisol, estrogen..etc
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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."


- 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

 

[Amazoniac]

Grapefruits that are not of bloody colors must have lower flavonoids content. The level of furadocouramids can also vary depending on the cultivar:
- Characterization of Furanocoumarin Profile and Inheritance Toward Selection of Low Furanocoumarin Seedless Grapefruit Cultivars
- Strategies to Produce Grapefruit-Like Citrus Varieties With a Low Furanocoumarin Content and Distinctive Flavonoid Profiles
- Breeding and Analysis of Two New Grapefruit-Like Varieties with Low Furanocoumarin Content

OPEN anesthesiology book , chapter 'What can my patient eat?' ,all there))

 

[IVILA]

The grapefruit contains high amounts furanocoumarin which is to cause the inhibition of cytochrome p450 enzyme.

This is where Ray confuses me/people at times. Oranges, which he is big on, has naringenin, and probably some of the other flavanoids.

Effect of Citrus Flavonoids, Naringin and Naringenin, on Metabolic Syndrome and Their Mechanisms of Action

Flavonoids are important natural compounds with diverse biologic activities. Citrus flavonoids constitute an important series of flavonoids. Naringin and its aglycone naringenin belong to this series of flavonoids and were found to display strong anti-inflammatory ...

www.ncbi.nlm.nih.gov

 

[Dave Clark]

The grapefruit contains high amounts furanocoumarin which is to cause the inhibition of cytochrome p450 enzyme.

Yes. I see that from the above literature, however, the Peat excerpt shows that he says naringenin modifies the metabolism of estrogen causing increased bioavailability of the estrogen. And , oranges, which he promotes, contains naringenin, so that is the confusing part. I think it has been pretty much established for a while now that grapefruit effects the cytochrome p450 enzyme, one reason why they recommend not to use it while taking drugs, since the drugs don't get broken down properly in the phase one detox system in the liver, and you can absorb more of the drug than normal.

 

[PeskyPeater]

Oh naringenin after ingestion is transformed to eriodictyol and has anti-estrogenic effects.

Intestinal microflora have been shown to further metabolize naringenin. Booth et al. (9) originally showed that oral doses of naringin administered to rats yielded 4-hydroxyphenylpropionic acid, 4-hydroxycinnamic acid, and 4-hydroxybenzoic acid sulfate in the urine. Griffiths and Smith (34) showed that rat intestinal microflora resulted in the generation of 4-hydroxyphenylpropionic acid and naringenin only, suggesting that 4-hydroxycinnamic acid and 4-hydroxybenzoic acid may be metabolites that are generated by hepatic enzymes. Honohan et al. (47) showed that the major intestinal metabolite of 3-[14C] hesperetin in rats was 3-phenylpropionic acid, while hepatic enzymes mediated further breakdown to benzoic acid and CO2..

The major metabolite observed for both naringenin and hesperetin was the flavonoid eriodictyol. Eriodictyol was generated by the addition of a hydroxy group to the R6 position of naringenin and the demethylation of the R6 methoxy of hesperetin. The hydroxylation of naringenin was shown to be mediated by hepatic cytochrome P450 1A (CYP1A) (74).

 

[Deleted member 5487]

Oh naringenin after ingestion is transformed to eriodictyol and has anti-estrogenic effects.

Thanks for the input

 

[Mossy]

Interesting thread.

My brother swears by grapefruit juice. He is definitely hypothyroid, prone to sickness, has kidney issues, and is a stage 4 cancer survivor. He says he feels immediate positive effects from grapefruit juice and eating grapefruits.

I barked the Peatism at him that grapefruits are pro-estrogen, anti-tyroid, but I think it's good to keep researching and discussing these things.

 

[liam183]

I drink it 50/50 with orange juice. I plan on just switching to OJ due to grapefruit's anti-thyroid nature

 

[PeskyPeater]

Habtemariam (37) examined the effect of flavonoids on TNFa– induced cytotoxicity in murine fibroblast L-929 cells. Although eriodictyol, a hepatic metabolite of naringenin, offered protection against TNF-induced cytotoxicity with an EC50 (50% effective concentration) of 4–6 µM, naringenin itself was not protective and actually potentiated the effect when examined at concentrations up to 250 µM.

Huang et al. (48) report that naringenin inhibits estrone sulfatase, a key enzyme in 17-b-estradiol synthesis, with an IC50 < 10 µM in human hepatic microsomes. Naringenin and hesperetin were found to inhibit rat hepatic microsomal glucuronidation of estrone and estradiol with an IC50 of approximately 25 µM (97). Relative to other flavonoids, naringenin and hesperetin were potent competitive inhibitors of estrone glucuronidation at a flavonoid concentration of 10 µM and noncompetitive inhibitors at a concentration of 50 µM.

Ruh et al. (82) showed that, in addition to its weakly in vitro estrogenic effects, (Fig. 6), naringenin exhibits antiestrogenic activity in vivo. In rats, naringenin (30 mg/rat) was shown to inhibit the 17-b-estradiol–induced increase in uterine weight, induction of progesterone receptor binding, [3 H]thymidine uptake, and uterine peroxidase activity. Naringenin also attenuated the estrogen-induced increase in cell proliferation in MCF-7 human breast cancer cells. These studies showed that, in addition to estrogenic effects, naringenin may significantly attenuate estrogenic activity. The balance between these two actions in vivo remains to be determined.

So... Eriodictyol is the flavonoids responsible for the positive effects of naringin / naringenin from citrus fruits.
Also found in peppermint.

 

[PeskyPeater]

I drink it 50/50 with orange juice. I plan on just switching to OJ due to grapefruit's anti-thyroid nature

Oh, the absorption of T4 is somewhat inhibited in the gut by grapefruit, but it is not inherently anti-thyroid.
Not much about 11-13% less

 

[PeskyPeater]

Dr peat is weird, he talks about naringenin in oranges, but it is actually hesperidin that is most rich in oranges and grapefruit is most rich in naringenin. Sometimes commercial orange juice is contaminated with naringenin though. -source
Yet another weird thing is, it seems that hesperitin the metabolite, is actually anti androgenic.

In addition to the estrogenic actions discussed above, naringenin may also act as a weak progestin. Rosenberg et al. (79) have shown that naringenin (10 muM) acts as a weak progestin in mammary cancer cell lines. Naringenin was approximately 104 -fold less potent than the agonist norgestrel. In contrast, the related flavanone hesperetin acts as an antiandrogen and antiprogestin at concentrations of 10 muM. The reason for the difference between naringenin and hesperetin, which are structurally quite similar, is unclear.

...of course we have to compare the in vivo effects to be sure.
anyhow as grapefruit has higher quercetin and kaempherol content than oranges, oranges are still supreme :)

 

[PeskyPeater]

OP you are cherry picking here, to show that alkalinity is a thing by increasing uptake of citrate, but it isn't a thing for it is highly difficult to change your state through diet because of multiple backup systems tightly regulating blood and cell pH.
And Dr Peat said the healthy metabolism of cells to be slightly on the acidic side because of the stream of carbonic acid, else when under stress, shifting to alkaline , they output the energy inefficient lactic acid which inhibit respiration and this alkalinity can cause cancer.

 

[PeskyPeater]

But increasing citrate is going to make you lose calcium which is regulating parathyroid hormone and leaving that unregulated is actually a factor in forming oxalate stones in the kidney. So the whole thing of potassium citrate pills is not making sense.

 

[PeskyPeater]

Proton pumps do not exist.