EDIT - clarification: the quotation of me in TheFountain's post above this one was actually written by oehaut.
Edited by Alex Libman, 07 April 2010 - 07:09 AM.
Posted 07 April 2010 - 06:58 AM
Edited by Alex Libman, 07 April 2010 - 07:09 AM.
Posted 07 April 2010 - 07:01 AM
Yes, but comparatively, are they superior to carnosine's antioxidant and anti-glycation capability, etc?I would say that higher antioxidant status is a possible causal rather than confounding factor. Your proposed study design doesn't take into account whole grain's or legumes considerable contribution to antioxidant levels.
Edited by Skotkonung, 07 April 2010 - 07:05 AM.
Posted 07 April 2010 - 07:02 AM
Yeah, I admit everything I wrote on this thread is uninformed politically-motivated subjective bunk.
Good job calling me on it.
Edited by Skotkonung, 07 April 2010 - 07:26 AM.
Posted 07 April 2010 - 07:11 AM
Posted 07 April 2010 - 07:20 AM
Posted 07 April 2010 - 12:03 PM
I always assumed that many vegetarians eat low quality vegetarian food - white bread, potato chips, pasta, cake etc. . . There are probably different types of vegetarians and it's hard to generalize about them as a group. I would guess that more healthy vegetarians tend to be those like Seventh Day Adventists, which have been studied to some extent. I know that does not address your desire for a high vegetable, fruit, and nut diet comparison with and without meat. I am just making a side comment.
Posted 07 April 2010 - 12:19 PM
Except that meat does not fall under the alkaline category.This is what all meat eater advocate here too
Regardless of this.only you add some oragnic grass-fed meat
There is correlative evidence that acidic foods may accelerate aging. And ray kurzweil advocates the alkaline diet, so there has to be something to it.
Theoretically, we humans should be better adapted physiologically to the diet our ancestors were exposed to during millions of years of hominid evolution than to the diet we have been eating since the agricultural revolution a mere 10,000 years ago, and since industrialization only 200 years ago. Among the many health problems resulting from this mismatch between our genetically determined nutritional requirements and our current diet, some might be a consequence in part of the deficiency of potassium alkali salts (K-base), which are amply present in the plant foods that our ancestors ate in abundance, and the exchange of those salts for sodium chloride (NaCl), which has been incorporated copiously into the contemporary diet, which at the same time is meager in K-base-rich plant foods. Deficiency of K-base in the diet increases the net systemic acid load imposed by the diet. We know that clinically-recognized chronic metabolic acidosis has deleterious effects on the body, including growth retardation in children, decreased muscle and bone mass in adults, and kidney stone formation, and that correction of acidosis can ameliorate those conditions. Is it possible that a lifetime of eating diets that deliver evolutionarily superphysiologic loads of acid to the body contribute to the decrease in bone and muscle mass, and growth hormone secretion, which occur normally with age? That is, are contemporary humans suffering from the consequences of chronic, diet-induced low-grade systemic metabolic acidosis? Our group has shown that contemporary net acid-producing diets do indeed characteristically produce a low-grade systemic metabolic acidosis in otherwise healthy adult subjects, and that the degree of acidosis increases with age, in relation to the normally occurring age-related decline in renal functional capacity. We also found that neutralization of the diet net acid load with dietary supplements of potassium bicarbonate (KHCO3) improved calcium and phosphorus balances, reduced bone resorption rates, improved nitrogen balance, and mitigated the normally occurring age-related decline in growth hormone secretion--all without restricting dietary NaCl. Moreover, we found that co-administration of an alkalinizing salt of potassium (potassium citrate) with NaCl prevented NaCl from increasing urinary calcium excretion and bone resorption, as occurred with NaCl administration alone. Earlier studies estimated dietary acid load from the amount of animal protein in the diet, inasmuch as protein metabolism yields sulfuric acid as an end-product. In cross-cultural epidemiologic studies, Abelow found that hip fracture incidence in older women correlated with animal protein intake, and they suggested a causal relation to the acid load from protein. Those studies did not consider the effect of potential sources of base in the diet. We considered that estimating the net acid load of the diet (i. e., acid minus base) would require considering also the intake of plant foods, many of which are rich sources of K-base, or more precisely base precursors, substances like organic anions that the body metabolizes to bicarbonate. In following up the findings of Abelow et al., we found that plant food intake tended to be protective against hip fracture, and that hip fracture incidence among countries correlated inversely with the ratio of plant-to-animal food intake. These findings were confirmed in a more homogeneous population of white elderly women residents of the U.S. These findings support affirmative answers to the questions we asked above. Can we provide dietary guidelines for controlling dietary net acid loads to minimize or eliminate diet-induced and age-amplified chronic low-grade metabolic acidosis and its pathophysiological sequelae. We discuss the use of algorithms to predict the diet net acid and provide nutritionists and clinicians with relatively simple and reliable methods for determining and controlling the net acid load of the diet. A more difficult question is what level of acidosis is acceptable. We argue that any level of acidosis may be unacceptable from an evolutionarily perspective, and indeed, that a low-grade metabolic alkalosis may be the optimal acid-base state for humans.
Steady-state plasma and urine acid-base composition was assessed in 19 studies of 16 normal subjects who ingested constant amounts of one of three diets that resulted in different rates of endogenous noncarbonic acid production (EAP) within the normal range. Renal net acid excretion (NAE) was used to quantify EAP since the two variables are positively correlated in normal subjects. A significant positive correlation was observed between plasma [H+] and plasma PCO2, and between plasma [HCO3-] and plasma PCO2, among the subjects. Multiple correlation analysis revealed a significant interrelationship among plasma [H+], plasma PCO2, and NAE (r = 0.71, P less than 0.001), and among plasma [HCO3-], plasma PCO2, and NAE (r = 0.77, P less than 0.001). The partial correlation coefficients indicated a significant positive correlation between plasma [H+] and NAE, and a significant negative correlation between plasma [HCO3-] and NAE, when plasma PCO2 was held constant. These findings indicate that two factors influence the level at which plasma [H+] is maintained in normal subjects: (1) the steady-state rate of endogenous noncarbonic acid production, and (2) the setpoint at which plasma PCO2 is regulated by the respiratory system. Plasma [HCO3-] is also co-determined by these two factors. In disease states, therefore, both factors must be known before a disturbance in acid-base homeostasis can be excluded.
The acid-ash hypothesis posits that protein and grain foods, with a low potassium intake, produce a diet acid load, net acid excretion (NAE), increased urine calcium, and release of calcium from the skeleton, leading to osteoporosis. The objectives of this meta-analysis were to assess the effect of changes in NAE, by manipulation of healthy adult subjects' acid-base intakes, on urine calcium, calcium balance, and a marker of bone metabolism, N-telopeptides. This meta-analysis was limited to studies that used superior methodological quality for the study of calcium metabolism. We systematically searched the literature and included studies if subjects were randomized to the interventions and followed the recommendations of the Institute of Medicine's Panel on Calcium and Related Nutrients for calcium studies. Five of 16 studies met the inclusion criteria. The studies altered the amount and/or type of protein. Despite a significant linear relationship between an increase in NAE and urinary calcium (p < 0.0001), there was no relationship between a change of NAE and a change of calcium balance (p = 0.38; power = 94%). There was no relationship between a change of NAE and a change in the marker of bone metabolism, N-telopeptides (p = 0.95). In conclusion, this meta-analysis does not support the concept that the calciuria associated with higher NAE reflects a net loss of whole body calcium. There is no evidence from superior quality balance studies 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.
Edited by oehaut, 07 April 2010 - 12:32 PM.
Posted 07 April 2010 - 04:49 PM
I've heard Ray Kurzweil paints his toe nails pink. Apparently there is correlative evidence that specimens with painted nails outlives those w/ more boring nails. YMMV, but this is interesting.There is correlative evidence that acidic foods may accelerate aging. And ray kurzweil advocates the alkaline diet, so there has to be something to it.
Edited by kismet, 07 April 2010 - 04:50 PM.
Posted 08 April 2010 - 08:49 AM
You are asking whether the antioxidant power of the carnosine in meat is greater than the phytochemicals in plant foods?Yes, but comparatively, are they superior to carnosine's antioxidant and anti-glycation capability, etc?I would say that higher antioxidant status is a possible causal rather than confounding factor. Your proposed study design doesn't take into account whole grain's or legumes considerable contribution to antioxidant levels.
Antioxidant activity of carnosine, homocarnosine, and anserine present in muscle and brain
"Carnosine, homocarnosine, and anserine are present in high concentrations in the muscle and brain of many animals and humans. However, their exact function is not clear. The antioxidant activity of these compounds has been examined by testing their peroxyl radical-trapping ability at physiological concentrations. Carnosine, homocarnosine, anserine, and other histidine derivatives all showed antioxidant activity. All of these compounds showing peroxyl radical-trapping activity were also electrochemically active as reducing agents in cyclic voltammetric measurements. Furthermore, carnosine inhibited the oxidative hydroxylation of deoxyguanosine induced by ascorbic acid and copper ions. Other roles of carnosine, such as chelation of metal ions, quenching of singlet oxygen, and binding of hydroperoxides, are also discussed. The data suggest a role for these histidine-related compounds as endogenous antioxidants in brain and muscle."
Carnosine and Carnosine-Related Antioxidants: A Review
"First isolated and characterized in 1900 by Gulewitsch, carnosine ( bgr-alanyl-L-hystidine) is a dipeptide commonly present in mammalian tissue, and in particular in skeletal muscle cells; it is responsible for a variety of activities related to the detoxification of the body from free radical species and the by-products of membrane lipids peroxidation, but recent studies have shown that this small molecule also has membraneprotecting activity, proton buffering capacity, formation of complexes with transition metals, and regulation of macrophage function. It has been proposed that carnosine could act as a natural scavenger of dangerous reactive aldehydes from the degradative oxidative pathway of endogenous molecules such as sugars, polyunsaturated fatty acids (PUFAs) and proteins. In particular, it has been recently demonstrated that carnosine is a potent and selective scavenger of agr,bgr-unsaturated aldehydes, typical by-products of membrane lipids peroxidation and considered second messengers of the oxidative stress, and inhibits aldehyde-induced protein-protein and DNA-protein cross-linking in neurodegenerative disorders such as Alzheimer's disease, in cardiovascular ischemic damage, in inflammatory diseases. The research for new and more potent scavengers for HNE and other agr,bgr-unsaturated aldehydes has produced a consistent variety of carnosine analogs, and the present review will resume, through the scientific literature and the international patents, the most recent developments in this field."
Meat is also rich in vitamin E, glutathione, selenium, and conjugated linoleic acid. Glutathione, a tripeptide (made of glutamate, cysteine, and glycine) is found mammalian cells and is a cofactor of glutathione peroxidase (GPx) an enzyme. It protects water-soluble proteins, detoxifies drugs, pollutants, poisons and oxidants such as hydrogen peroxide, and dehydroascorbic acid.
When classifying the samples into the three main classes the difference in antioxidant content between plant- and animal-based foods become apparent. The results here uncover that the antioxidant content of foods varies several thousand-fold and that antioxidant rich foods originate from the plant kingdom while meat, fish and other foods from the animal kingdom are low in antioxidants. Comparing the mean value of the 'Meat and meat products' category with plant based categories, fruits, nuts, chocolate and berries have from 5 to 33 times higher mean antioxidant content than the mean of meat products. Diets comprised mainly of animal-based foods are thus low in antioxidant content while diets based mainly on a variety of plant-based foods are antioxidant rich, due to the thousands of bioactive antioxidant phytochemicals found in plants which are conserved in many foods and beverages.
Edited by Application, 08 April 2010 - 09:03 AM.
Posted 08 April 2010 - 09:09 AM
Yes, but you're missing the point. Meat and animal products also provide other benefits, such as inhibiting glycation, etc. Obviously, vegetarians / vegans have higher plasma AGES (one, two). Surely many plants contain glycation inhibitors as well (ECGC for instance), but they don't appear to work as well as carnosine in the context of a meat containing diet. And context is important in an open system like the human body. The additional benefits of meat / animal products exist in addition to their antioxidant capabilities and may have a synergistic effect with plant borne compounds. Not to mention, just because a food has a high antioxidant status, it doesn't necessarily translate to superior endogenous antioxidant capability or reduction of disease (note the vegetables / fruit only modestly reduce cancer post). The Inuit, which consume an entirely meat based diet, have significantly lower rates of cancer than their Western contemporaries. Using your conventional wisdom, without the benefits of fruits and vegetables, one would assume this couldn't be possible. Furthermore, back to my original nutri-genomics post, some people cannot utilize beta-carotene (a supposedly potent antioxidant). Once can only speculate that this extends to other substances as well.You are asking whether the antioxidant power of the carnosine in meat of meat is greater than the phytochemicals in plant foods?
In my limited reading on the subject, I didn't see any evidence that carnosine is qualitatively superior to plant derived dietary antioxidants. Did you? On the other hand, It seems pretty universally accepted that total measurable antioxidant levels are much higher in all kinds of plant foods. Among many examples, this study published in 2010 found:When classifying the samples into the three main classes the difference in antioxidant content between plant- and animal-based foods become apparent. The results here uncover that the antioxidant content of foods varies several thousand-fold and that antioxidant rich foods originate from the plant kingdom while meat, fish and other foods from the animal kingdom are low in antioxidants. Comparing the mean value of the 'Meat and meat products' category with plant based categories, fruits, nuts, chocolate and berries have from 5 to 33 times higher mean antioxidant content than the mean of meat products. Diets comprised mainly of animal-based foods are thus low in antioxidant content while diets based mainly on a variety of plant-based foods are antioxidant rich, due to the thousands of bioactive antioxidant phytochemicals found in plants which are conserved in many foods and beverages.
Edited by Skotkonung, 08 April 2010 - 09:17 AM.
Posted 08 April 2010 - 09:42 AM
Yes, but you're missing the point. Meat and animal products also provide other benefits, such as inhibiting glycation, etc. Obviously, vegetarians / vegans have higher plasma AGES (one, two). Surely many plants contain glycation inhibitors as well (ECGC for instance), but they don't appear to work as well as carnosine in the context of a meat containing diet. And context is important in an open system like the human body. The additional benefits of meat / animal products exist in addition to their antioxidant capabilities and may have a synergistic effect with plant borne compounds. Not to mention, just because a food has a high antioxidant status, it doesn't necessarily translate to superior endogenous antioxidant capability or reduction of disease (note the vegetables / fruit only modestly reduce cancer post). The Inuit, which consume an entirely meat based diet, have significantly lower rates of cancer than their Western contemporaries. Using your conventional wisdom, without the benefits of fruits and vegetables, one would assume this couldn't be possible. Furthermore, back to my original nutri-genomics post, some people cannot utilize beta-carotene (a supposedly potent antioxidant). Once can only speculate that this extends to other substances as well.
This is the point I am trying to make: Is a animal protein + vegetable / fruit diet superior to a vegetable protein + vegetable / fruit diet, if both diets contain equal calories and fruits / vegetables? Are we losing some synergy or creating micronutrient deficiencies when we remove meat? If we really want to know which diet is better un-supplemented, then these are the questions that need to be asked.
Edited by Application, 08 April 2010 - 09:52 AM.
Posted 08 April 2010 - 12:48 PM
This is the point I am trying to make: Is a animal protein + vegetable / fruit diet superior to a vegetable protein + vegetable / fruit diet, if both diets contain equal calories and fruits / vegetables? Are we losing some synergy or creating micronutrient deficiencies when we remove meat? If we really want to know which diet is better un-supplemented, then these are the questions that need to be asked.
Posted 08 April 2010 - 02:04 PM
Edited by NDM, 08 April 2010 - 02:06 PM.
Posted 08 April 2010 - 05:21 PM
Definitively, I think we can make the supposition that an un-supplemented strict vegetarian, particularly vegan, diet will cause micro-nutrient deficiencies. Lack of B12 will cause homocystein to rise, lack of taurine and other similar compounds may cause excess glycation. I've seen some studies indicating zinc (and several other minerals), sufficient n3 PUFA, and iodine could be lacking [source]. Likely these problems are indicative of sub-optimal health.This is the point I am trying to make: Is a animal protein + vegetable / fruit diet superior to a vegetable protein + vegetable / fruit diet, if both diets contain equal calories and fruits / vegetables? Are we losing some synergy or creating micronutrient deficiencies when we remove meat? If we really want to know which diet is better un-supplemented, then these are the questions that need to be asked.
Exactly this. But now, how are we gonna answer this? There is never gonna have such study, and we are left with mechanecal speculation or prospective data that don't apply to our context. TO be fair, if we're base on this (epidemiology and in vitro), it would looks like vegan diet is superior to a diet containing meat.
As kismet said, it more or less looks to me like a bet right now.
Posted 20 May 2010 - 02:34 PM
Posted 20 May 2010 - 06:03 PM
Definitively, I think we can make the supposition that an un-supplemented strict vegetarian, particularly vegan, diet will cause micro-nutrient deficiencies.
So, I think we can conclude that an un-supplemented diet for vegan, and possibly vegetarian, is sub-optimal. Lacto-ovo vegetarian is probably not at risk.
Posted 20 May 2010 - 07:11 PM
Posted 20 May 2010 - 08:06 PM
Posted 20 May 2010 - 08:26 PM
Actually, I think there is, but it depends whether we talk about average intakes of vegetarians, deficient vs sub-optimal/marginal, what is a supplement? (fortified foods, targeted consumption of specific foods, extracts and isolates, etc), general or life extension "LE" vegetarian diets (which even if they're 'ovo-lacto' in many cases will contain max. 1 egg/d and mostly low fat dairy; to me that's a "usual" LE veg* diet), ad lib or CR, how we define 'micronutrient', other standards we want to apply, ...this is absolutely not true, there is -no- evidence that suggests that [ovo-lacto] vegetarian diets are lacking in any MN. comparing a vegetarian diet to a vegan diet is almost as far fetched as comparing a omnivorous diet to a vegetarian diet. vegan diets have significant risk of MN deficiency but [healthy] vegetarian diets do NOT.
Edited by kismet, 20 May 2010 - 08:45 PM.
Posted 20 May 2010 - 09:21 PM
Posted 20 May 2010 - 10:33 PM
Edited by hypnotoad, 20 May 2010 - 10:40 PM.
Posted 20 May 2010 - 10:42 PM
Posted 20 May 2010 - 11:08 PM
It is probably safe to assume that the average vegetarian, whether of the 'junkfood' or 'healthy' diet variety, will suffer from a range of imbalances and modest deficiencies without using CRON-o-meter, just different ones compared to omnivorous diets.
The reason I am doing an aqua-vegetarian diet at this time (including some seafood) is because I simply cannot afford the exotic protein sources of a full fledged vegan diet.
Edited by ajnast4r, 20 May 2010 - 11:11 PM.
Posted 20 May 2010 - 11:29 PM
consuming animal flesh in any form excludes your from being a vegetarian. aqua-vegetarian or pescetarian are misnomers.... there is no such thing. consuming flesh, in any form, makes you an omnivore.
Edited by hypnotoad, 20 May 2010 - 11:34 PM.
Posted 21 May 2010 - 02:43 AM
Edited by Forever21, 21 May 2010 - 03:26 AM.
Posted 21 May 2010 - 03:16 AM
Yeah, I admit everything I wrote on this thread is uninformed politically-motivated subjective bunk.
Good job calling me on it.
Debunked. Next!
You might reconsider green tea. Evidence in its favor is substantial. Just drink more water or find a decaffeinated brand if you are concerned about the diuretic effects.
Posted 21 May 2010 - 07:05 AM
Posted 21 May 2010 - 07:59 AM
What the hell? A vegetarian that eats dairy, eggs and fish?
Why not just call yourself a non-meat eater? That seems more accurate to me.
Calling yourself a vegetarian, while eating fish and eggs is extremely hypocritical in my opinion.
Posted 21 May 2010 - 08:07 AM
Edited by Skötkonung, 21 May 2010 - 08:09 AM.
Posted 21 May 2010 - 08:22 AM
While I love the low-carb paleo style diet, I wouldn't prescribe it to my 60-something parents.
I think a diet with a lot of wild caught fish, lots of leafy greens, naturally occurring animal and plant fats, some nuts, low-sugar fruit and berries, and nutrient rich tubers is probably ideal. Throw in some raw dairy / artisan cheese for good measure.
That's the route I've been pushing my parents. I've got them switch out white potato for sweet potatoes, some canola oil based spread for organic pastured butter, and to ditch the sodium and preservative laden processed meats. No more bread at dinner and to do a steak salad for lunch. One step at a time I guess. It has already done wonders for my mothers lipid profile.
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