WHERE DID PROTEIN & BONE-LOSS THEORY ORIGINATE FROM?
Acc. to a 2008 study in the American Journal of Clinical Nutrition, by US researchers Robert Heaney & Donald Layman , there are many factors that influence bone mass, but protein has been identified as being both detrimental and beneficial to bone health, depending on a variety of factors, including the level of protein in the diet, the protein source, calcium intake, weight loss, and the acid/base balance of the diet. Protein intake affects bone in several ways: 1) it provides the structural matrix of bone, 2) it optimizes IGF-1 levels, 3) it is reported to increase urinary calcium, and 4) it is reported to increase intestinal calcium absorption.
Moreover, loss of bone mass (osteopenia) and loss of muscle mass (sarcopenia) that occur with age are closely related. Factors that affect muscle anabolism, including protein intake, also affect bone mass. Bone health is not simply a skeletal issue; it is a musculoskeletal issue.
The high protein content of Western diets is often cited as a risk factor for osteoporosis or bone fractures. In a 1990 study in the Journal of Nutrition, US researchers, J.E. Kerstetter & L.H. Allen, concluded from the available literature at that time that, calcium and phosphorus intakes typically consumed by the American adult, increases in dietary protein do increase urinary Ca, resulting in a shift of Ca balance in a negative direction.
US researchers L.K. Massey & U.S. Barzel, in a 1998 study in the Journal of Nutrition , suggested that, the average American diet, which is high in protein and low in fruits and vegetables, generates a large amount of acid, mainly as sulphates and phosphates. The kidneys respond to this dietary acid challenge with net acid excretion. Concurrently, the skeleton supplies buffer by active resorption of bone. Indeed, calciuria is directly related to net acid excretion. Different food proteins differ greatly in their potential acid load, and therefore in their acidogenic effect. A diet high in acid-ash proteins causes excessive calcium loss because of its acidogenic content. The addition of exogenous buffers, as chemical salts or as fruits and vegetables, to a high protein diet results in a less acid urine and a reduction in net acid excretion. Alkali buffers, whether chemical salts or dietary fruits and vegetables high in potassium, reverse acid-induced urinary calcium loss.
Earlier studies suggested that, as a result of increased urinary calcium excretion with high protein intake, there is an increased risk of fractures or osteoporosis. As protein intake increases, there is an increase in urinary calcium, with most subjects developing negative calcium balance
In a 1974 study in the American Journal of Clinical Nutrition, researcher Dr. S. Margen & team, found a positive correlation between protein ingestion and calciuria. “Although the response was not linear, varying protein intake from 0g to 90g/day results in approximately an 800% increase in calcium excretion, irrespective of calcium intake. This effect of protein occurred in all our studies of individuals, and was also observed with pure L-amino acid mixtures”, found the researchers.
In a 1983 study in the American Journal of Clinical Nutrition, researcher J.M. Bengoa & team, gave intravenous amino acids to five patients, at the rate of 1-2g/kg of body weight. Researchers found that, as the urinary amino acid dose increased, the urinary calcium excretion increased. It was thus concluded that, hypercalciuria induced by high levels of amino acid infusion during total parenteral nutrition may contribute to the development of metabolic bone disease.
Two famous epidemiological studies which pushed the hypothesis of high protein intake and its association with bone loss, were:
Now, a major limitation of both studies was the use of a mailed food- frequency questionnaire on a limited number of occasions and limited evaluation of other lifestyle and dietary factors that may have contributed to fracture risk.
Though later, the acid-ash hypothesis or the protein-calcium loss theory, was debunked, there were many later studies, which raised doubts in terms of certain specific situations.
In a 2008 study in the Journal of Bone & Mineral Research, a French research team, led by Patricia D. Molina, determined whether the association between protein intake and the overall acid-base equilibrium of the diet and fracture risk vary according to calcium intake. Researchers observed women from the famous E3N study in France, which was initiated in France in 1990 to study the risk factors for the most frequent sites of cancer in over 100,000 women, living in France, 40–65yr of age. The researchers studied, over 36,000 postmenopausal women, of which over 2,400 reported a fracture (excluding high-impact trauma).
Researchers found no overall association between fracture risk and total protein. However, in the lowest intake of calcium (<400 mg/1000 kcal), high protein intake was associated with a significant increased fracture risk. An increasing fracture risk with increasing animal protein intake was also observed.
In a 2016 study in the journal Applied Physiology, Nutrition & Metabolism, by a research team led by German researcher Martina Heer , tested the regimen of high protein intake, applied during bed rest with calcium and potassium intake meeting recommended values, would prevent any effect of bed rest on bone turnover. 16 women on bed rest, were divided into two groups: Control (CON) subjects received 1g/kg body mass/d dietary protein. High protein subjects received 1.45g protein/kg body mass/d plus an additional 0.72g branched-chain amino acids (BCAA) per day during bed rest. All subjects received an individually tailored diet, with the control group’s diet being higher in fat and carbohydrate intake.
Researchers found that high protein intake in bed rest might exaggerate bone loss. Data suggest that the higher protein intake increased osteoclast activity and might exacerbate long-term risk for bone loss in bed-ridden people.
A team of US researchers led by D.E. Sellmeyer, in the 2001 study in the American Journal of Clinical Nutrition , found that, elderly women with a high dietary ratio of animal to vegetable protein intake have more rapid femoral neck bone loss and a greater risk of hip fracture than do those with a low ratio. This suggests that an increase in vegetable protein intake and a decrease in animal protein intake may decrease bone loss and the risk of hip fracture.
THE ACID-ASH HYPOTHESIS
In my ebook and related video on “The Myth of Alkaline Water” (Video Link 1 and video link 2, where I busted the myth of alkaline water and alkaline diet, which is based on the acid-alkaline hypothesis, which made people earn a quick buck by convincing others of this false theory. It is surely true that the foods we eat will change the ph of our urine. That’s why having a green smoothie will make your pee alkaline, when you check it with a ph strip. This gives the people an instant happiness and conviction to not just continue with whatever myth they are following, but also recommend it to others.
But, we saw that a change in urinary ph does not mean a change in blood ph, which is very tightly regulated by the body. The changes in blood ph can only be in case of a serious kidney issue. So, having a chicken or a salad, won’t make much of a difference to your blood ph.
Another common hypothesis linked to the acid-alkaline hypothesis is called the ‘acid-ash hypothesis of osteoporosis’, acc. to which the body draws minerals like calcium, magnesium etc. from the bones, thus leading to osteoporosis in the long run. However, studies have already debunked this myth.
Acc. to a 2011 meta-analysis study in the Nutrition Journal, Canadian researcher Tanis R. Fenton & team ,acid-ash hypothesis means that high dietary protein intakes are detrimental to bone health since protein is an important “acid generating” diet component, and structural bone mineral is dissolved to release bicarbonate to neutralize acid and avoid acidosis.
Fenton & team, carried out a meta-analysis of over fifty-five studies, where the acid-ash or acid-base diet hypothesis with bone-related outcomes, in which the diet acid load was altered, or an alkaline diet or alkaline salts were provided, to healthy human adults.
They found that, urine calcium excretion rates were consistent with osteoporosis development; however, calcium balance studies did not demonstrate loss of whole body calcium with higher net acid excretion. No studies provided direct evidence of osteoporosis progression (fragility fractures, or bone strength as measured using biopsy). The supporting studies were not controlled regarding important osteoporosis risk factors including: weight loss during follow-up, family history of osteoporosis, baseline bone mineral density, and estrogen status. No study revealed a biologic mechanism functioning at physiological pH. Finally, studies did not provide evidence for an adverse role of phosphate, milk, and grain foods in osteoporosis.
Acc. to author and researcher Chris Kresser , “The kidneys are well equipped to deal with ‘acid ash.’ When we digest things like protein, the acids produced are quickly buffered by bicarbonate ions in the blood. This reaction produces carbon dioxide, which is exhaled through the lungs, and salts, which are excreted by the kidneys. During the process of excretion, the kidneys produce ‘new’ bicarbonate ions, which are returned to the blood to replace the bicarbonate that was initially used to buffer the acid. This creates a sustainable cycle in which the body is able to maintain the pH of the blood, with no involvement from the bones whatsoever.”
In a 2014 study in the journal Critical Reviews in Food Science & Nutrition, German researcher T. Remer & team, suggested that, although in the past high protein intake was often assumed to exert a primarily detrimental impact on bone mass and skeletal health, the majority of recent studies indicate the opposite and suggests a bone-anabolic influence. Studies examining the influence of alkalizing diets or alkalizing supplement provision on skeletal outcomes are less consistent, which raises doubts about the role of acid-base status in bone health.
US researcher J.J. Cao in a 2017 study in the journal Current Osteoporosis Reports , found that, epidemiological studies show that long-term, high-protein intake is positively associated with bone mineral density and reduced risk of bone fracture incidence. Short-term interventional studies demonstrate that a high-protein diet does not negatively affect calcium homeostasis. Existing evidence supports that the negative effects of the acid load of protein on urinary calcium excretion are offset by the beneficial skeletal effects of high-protein intake.
A 2009 meta-analysis of over 16 studies, in the Journal of Bone & Mineral Research, by a Canadian research team, led by Tanis R. Fenton , assessed the effect of changes in net acid accretion, by manipulation of healthy adult subjects’ acid-base intakes, on urine calcium, calcium balance, and a markers of bone metabolism.
Researchers found that, despite a significant linear relationship between an increase in net acid accretion and urinary calcium, there was no relationship between a change of net acid accretion and a change of calcium balance. There was no relationship between a change of net acid accretion and a change in the marker of bone metabolism. Thus, this meta-analysis did not support the concept that the calciuria associated with higher net acid accretion reflects a net loss of whole body calcium. There is no evidence that increasing the diet acid load promotes skeletal bone mineral loss or osteoporosis. Changes of urine calcium do not accurately represent calcium balance. Promotion of the ‘‘alkaline diet’’ to prevent calcium loss is not justified.
Acc. to a 2011 study in the journal Current Opinion in Lipidology, by US researcher Jane E. Kerstetter & team, undoubtedly, an increase in dietary protein results in greater urinary calcium. What has been unclear up to this point is the source of the urinary calcium. The traditional hypothesis was that a high intake of protein, particularly from animal sources, generates a high fixed metabolic acid load because the animal proteins contain higher amounts of sulphur-containing amino acids. Should the kidneys and lungs be unable to completely handle the diet-induced acid load, a source of additional buffer would be necessary via osteoclast-activated bone resorption. The large bicarbonate reservoir of the skeleton would provide this buffer; calcium would consequently be released from bone with the carbonate.
Researchers found that, many studies have found a significant positive relationship between protein intake and bone mass or density. Similarly, various studies in humans have also demonstrated greater calcium retention and absorption by individuals consuming high-protein diets, particularly when the calcium content of the diet was limiting. High-protein intake may positively impact bone health by several mechanisms, including calcium absorption, stimulation of the secretion of insulin-like growth factor-1, and enhancement of lean body mass. The concept that an increase in dietary protein induces a large enough shift in systemic pH to increase osteoclastic bone resorption seems untenable.
One of the most extensive studies on this topic was the 2013 study in the British Journal of Nutrition, by Swiss researcher Jean-Philippe Bonjour. Bonjour concluded in the study by saying: “several recent human studies have shown that there is no relationship between nutritionally induced variations of urinary acid excretion and Ca balance, bone metabolism and the risk of osteoporotic fractures. Variations in human diets across a plausible range of intakes have been shown to have no effect on blood pH… long-term studies of alkalinising diets have shown no effect on the age-related change in bone fragility. Consequently, advocating the consumption of alkalinising foods or supplements and/or removing animal protein from the human diet is not justified by the evidence accumulated over the last several decades.”
LET’S BUST THE MYTH
British researcher Fiona Ginty, in the 2003 study in the journal Proceedings of the Nutrition Society, suggested that, over the last 80 years numerous studies have demonstrated that a high protein intake increases urinary Ca excretion and that on average 1mg Ca is lost in urine for every 1g rise in dietary protein. This relationship is primarily attributable to metabolism of Sulphur amino acids present in animal and some vegetable proteins, resulting in a greater acid load and buffering response by the skeleton.
However, suggested Ginty, that many of these early studies that demonstrated the calciuric effects of protein were limited by low subject numbers, methodological errors and the use of high doses of purified forms of protein. Furthermore, the cross-cultural and population studies that showed a positive association between animal-protein intake and hip fracture risk did not consider other lifestyle or dietary factors that may protect or increase the risk of fracture. The effects of protein on bone appear to be biphasic and may also depend on intake of Ca- and alkali-rich foods, such as fruit and vegetables. At low protein intakes insulin-like growth factor production is reduced, which in turn has a negative effect on Ca and phosphate metabolism, bone formation and muscle cell synthesis.
Acc. to Heaney & Layman, despite a widely held belief that high-protein diets (especially diets high in animal protein) result in bone resorption and increased urinary calcium, higher protein diets are actually associated with greater bone mass and fewer fractures when calcium intake is adequate.
Among the 72 premenopausal women studied, there was a statistically significant positive association between protein intake and bone mineral in the distal radius and proximal femur, which was not altered by adjustment for age, weight, and physical activity. Results suggest that dietary protein intake may be a determinant of the peak bone mass attained by premenopausal white women.
Researchers saw that, compared with controls, patients who received protein supplements had significantly greater increases in serum levels of insulin-like growth factor-I, and an attenuation of the decrease in proximal femur bone mineral density. Thus, researchers found that, protein repletion after hip fracture was associated with increased serum levels of insulin-like growth factor-I, attenuation of proximal femur bone loss, and shorter stay in rehabilitation hospitals.
Researchers found that, the risk of hip fracture was not related to intake of calcium or vitamin D, but was negatively associated with total protein intake. Animal rather than vegetable sources of protein appeared to account for this association. Thus, intake of dietary protein, especially from animal sources, may be associated with a reduced incidence of hip fractures in postmenopausal women.
Researchers found that, lower protein intake was significantly related to bone loss at femur and spine. Persons with the lowest protein intake showed the greatest bone loss. Similar to the overall protein effect, lower percent animal protein also was significantly related to bone loss. Thus, women and men with relatively lower protein intake had increased bone loss, suggesting that protein intake is important in maintaining bone or minimizing bone loss in elderly persons.
Researchers found that, higher protein intake was significantly associated with a favourable 3yr change in total-body BMD in the supplemented group but not in the placebo group. Thus, increasing protein intake may have a favourable effect on change in bone mineral density in elderly subjects supplemented with calcium citrate malate and vitamin D.
The study showed that there is a strong positive association between bone mineralization and dietary protein. In the study, long-term increase in dietary-protein content did not increase the loss of BMC; in fact, bone mineral mass was relatively better preserved during weight loss achieved during the high-protein intake. Researchers therefore conclude that a high dietary-protein intake does not seem to have adverse effects on bone mineralization in healthy individuals undergoing major weight loss.
Researchers found that, the diets did not affect urinary calcium loss or indicators of bone metabolism. In conclusion, under controlled conditions, a high meat compared with a low meat diet for 8wk did not affect calcium retention or biomarkers of bone metabolism in healthy postmenopausal women. Calcium retention is not reduced when subjects consume a high protein diet from common dietary sources such as meat.
Researchers found that, high compared with low dietary protein significantly increased calcium retention from the low-calcium but not the high-calcium diet. Testing at 1, 2, 3, 5, and 7wk showed no long-term adaptation in urinary acidity or urinary calcium excretion. High compared with low dietary protein increased serum insulin-like growth factor I. Thus, in healthy postmenopausal women, a moderate increase in dietary protein, from 10% to 20% of energy, slightly improved calcium absorption from a low-calcium diet, nearly compensating for a slight increase in urinary calcium excretion.
Therefore, concluded the researchers, consuming protein (including that from meat) higher than current Recommended Dietary Allowance for protein is beneficial to calcium utilization and bone health, especially in the elderly. A high-protein diet with adequate calcium and fruits and vegetables is important for bone health and osteoporosis prevention.
Results from middle-aged men and women show that higher animal protein intake coupled with calcium intake of 800mg/day or more may protect against hip fracture, whereas the effect appears reversed for those with lower calcium intake. Calcium intake modifies the association of protein intake and the risk of hip fracture.
Compared with the placebo group, the protein group had significantly higher serum IGF-1 level at 1 and 2 years. The study showed that in protein-replete healthy ambulant women, 30g of extra protein increased IGF-1 but did not have beneficial or deleterious effects on bone mass or strength. The effect of protein supplementation in populations with low dietary protein intake requires urgent attention.
Researchers found that, increased protein intake was associated with a decreased risk of hip fracture compared to those in the lowest quartile of protein intake. When a threshold effect was considered, intakes in the higher quartiles combined were associated with a significantly lower risk for hip fracture.
Researchers found that, higher dietary protein intakes were associated with reduced odds of falling. Higher intakes of total, animal and plant protein showed a significantly lower rate of subsequent falls. This work highlights the importance of adequate protein intake as a potentially modifiable risk factor for fall prevention in older adults.
Researchers found that, hypo-energetic diets higher in dairy foods, dietary calcium, and protein with daily exercise, favourably affected important bone health biomarkers vs. diets with less of these bone-supporting nutrients.
The net difference between the amount of Ca absorbed and excreted in urine did not differ between 2 diet periods. The dietary treatments did not affect other markers of bone metabolism. In summary, a diet high in protein and PRAL increases the fractional absorption of dietary Ca, which partially compensates for increased urinary Ca, in postmenopausal women. This indicates that a high-protein diet has no adverse effects on bone health.
Researchers found that, in both sexes, the group with the highest protein intake had significantly lower odds of developing lumber osteoporosis when compared to the group with the lowest protein intake.
The analysis showed that, bone health is a multifactorial musculoskeletal issue, and optimal protein intakes are key in developing and maintaining bone throughout the life span. High vs low protein intakes resulted in a statistically significant 16% decrease in hip fractures. Data from studies included in these analyses collectively lean toward the hypothesis that protein intake above the current RDA is beneficial to BMD at several sites. There were no differences between animal or plant proteins.
In older people with osteoporosis, higher protein intake (≥0.8-g/kg/day, i.e., above the current RDA) is associated with higher BMD, a slower rate of bone loss, and reduced risk of hip fracture, provided that dietary calcium intakes are adequate. Dietary protein supplements attenuate age-related BMD decrease and reduce bone turnover marker levels, together with an increase in IGF-I and a decrease in PTH. There is no evidence that diet-derived acid load is deleterious for bone health. Thus, insufficient dietary protein intakes may be a more severe problem than protein excess in the elderly.
During the 6-month treatment period, there was a significant difference in protein intake between the control and high-protein groups; however, there were no differences in the consumption total calories, carbohydrate or fat. Whole body bone mineral density did not change in the control or high-protein group. Similarly, lumbar bone mineral density did not change in the control or high-protein group. Furthermore, there were no changes in fat mass or lean body mass. Thus, despite an 87% higher protein intake (high-protein versus control), 6 months of a high-protein diet had no effect on whole body bone mineral density, lumbar bone mineral density, T-scores, lean body mass or fat mass.
Researchers found no significant changes for any measure of body composition over the course of the year (i.e., body weight, fat mass, lean body mass, percent fat, whole body bone mineral content, whole body T-score, whole body bone mineral density, lumbar bone mineral content, lumbar bone mineral density and lumbar T-score). In addition, no adverse effects on kidney function was seen. Based on this 1-year investigation, it is evident that a diet high in protein has no adverse effects on bone mineral density or kidney function.
Akshay Chopra is a renowned fitness professional, a speaker , a writer and the owner of Indias research based platform, Werstupid. He has been transforming lives, and has addressed many a people with motivational words. Known as the Encyclopaedia of Fitness Industry, his knowledge is unparalleled.
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