Why one meal a day?

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tattoogunman
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Re: Why one meal a day?

Post by tattoogunman »

samseva wrote:
tattoogunman wrote:Yes, but a baby's nutritional requirements versus those of an adult are completely different ;)
A baby's nutritional requirements vary in nutritional quantities compared to those of an adult—in large part due to its size—but it is basically the exact same micro- and macronutrients. Even if this statement were true, the fact that adults would have different nutritional requirements than babies would in no way make saturated fat unhealthy.
I never said it was, just that a baby's requirements are different from those of an adult. All things in moderation... ;)
daverupa
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Re: Why one meal a day?

Post by daverupa »

samseva wrote:
tattoogunman wrote:Yes, but a baby's nutritional requirements versus those of an adult are completely different ;)
A baby's nutritional requirements vary in nutritional quantities compared to those of an adult—in large part due to its size—but it is basically the exact same micro- and macronutrients.
False.

http://www.livestrong.com/article/44116 ... s-of-life/
Babies grow at a faster rate than people at any other stage of life. Because of this phenomenal growth, your infant's nutritional needs are different from those of an adult or older child. In addition, the rapid development of your baby's brain means he needs more of particular nutrients, but his small size requires that you provide some nutrients in smaller quantities.
  • "And how is it, bhikkhus, that by protecting oneself one protects others? By the pursuit, development, and cultivation of the four establishments of mindfulness. It is in such a way that by protecting oneself one protects others.

    "And how is it, bhikkhus, that by protecting others one protects oneself? By patience, harmlessness, goodwill, and sympathy. It is in such a way that by protecting others one protects oneself.

- Sedaka Sutta [SN 47.19]
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Alex123
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Re: Why one meal a day?

Post by Alex123 »

Still,

Adults nad babies, are humans. We do need similar kind of nutrients, just in different amount and/or proportions.
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samseva
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Re: Why one meal a day?

Post by samseva »

daverupa wrote:False.

http://www.livestrong.com/article/44116 ... s-of-life/
Babies grow at a faster rate than people at any other stage of life. Because of this phenomenal growth, your infant's nutritional needs are different from those of an adult or older child. In addition, the rapid development of your baby's brain means he needs more of particular nutrients, but his small size requires that you provide some nutrients in smaller quantities.
Live Strong is almost as reliable as Lance Armstrong himself. That aside, I said the nutritional requirements vary is quantity, but are the exact same micro- and macro-nutrients as the nutritional requirements of adults, which is what the article you posted describes.
daverupa
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Re: Why one meal a day?

Post by daverupa »

Nevermind; talking nutrition with people is as foolish as talking with them about post-death speculations & politics; I forget this, sometimes.
  • "And how is it, bhikkhus, that by protecting oneself one protects others? By the pursuit, development, and cultivation of the four establishments of mindfulness. It is in such a way that by protecting oneself one protects others.

    "And how is it, bhikkhus, that by protecting others one protects oneself? By patience, harmlessness, goodwill, and sympathy. It is in such a way that by protecting others one protects oneself.

- Sedaka Sutta [SN 47.19]
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samseva
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Re: Why one meal a day?

Post by samseva »

daverupa wrote:Nevermind; talking nutrition with people is as foolish as talking with them about post-death speculations & politics; I forget this, sometimes.
Yes, it is surprising how emotionally-charged of a topic it is.

No hard feelings, though. :smile:
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Mkoll
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Re: Why one meal a day?

Post by Mkoll »

daverupa wrote:talking nutrition with people is as foolish as talking with them about post-death speculations & politics
Depends on who you're talking to, but true in most cases IME.
Namo tassa bhagavato arahato samma sambuddhassa
Namo tassa bhagavato arahato samma sambuddhassa
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Mkoll
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Re: Why one meal a day?

Post by Mkoll »

samseva wrote:The problem is not cholesterol itself, it is oxidized cholesterol that is unhealthy. Oxidization of cholesterol—one among many other foods that can be oxidized—happens especially when cholesterol is cooked, even at low temperatures.
If oxidized cholesterol is unhealthy...and dairy, eggs, meat, and fish contain oxidized cholesterol (which they do)...then dairy, eggs, meat, and fish are unhealthy.

:thinking:
Namo tassa bhagavato arahato samma sambuddhassa
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samseva
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Re: Why one meal a day?

Post by samseva »

Mkoll wrote:
samseva wrote:The problem is not cholesterol itself, it is oxidized cholesterol that is unhealthy. Oxidization of cholesterol—one among many other foods that can be oxidized—happens especially when cholesterol is cooked, even at low temperatures.
If oxidized cholesterol is unhealthy...and dairy, eggs, meat, and fish contain oxidized cholesterol (which they do)...then dairy, eggs, meat, and fish are unhealthy.

:thinking:
A small quantity of oxidized cholesterol doesn't make an entire food unhealthy. The logic doesn't add up and it could be applied to any food with minute amounts of unhealthy or inedible compounds; making almost anything we eat unhealthy.

More so, eggs can be cooked without cooking the cholesterol and there are cuts of meat which have much lower fat content, and therefore cholesterol.
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Mkoll
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Re: Why one meal a day?

Post by Mkoll »

samseva wrote:
Mkoll wrote:
samseva wrote:The problem is not cholesterol itself, it is oxidized cholesterol that is unhealthy. Oxidization of cholesterol—one among many other foods that can be oxidized—happens especially when cholesterol is cooked, even at low temperatures.
If oxidized cholesterol is unhealthy...and dairy, eggs, meat, and fish contain oxidized cholesterol (which they do)...then dairy, eggs, meat, and fish are unhealthy.

:thinking:
A small quantity of oxidized cholesterol doesn't make an entire food unhealthy. The logic doesn't add up and it could be applied to any food with minute amounts of unhealthy or inedible compounds; making almost anything we eat unhealthy.
The dose makes the poison. Eating a little bit of unhealthy stuff once in awhile probably isn't going to lead to disease. But eating it regularly may. It's chronic habits that lead to chronic disease.

Oxidized cholesterol is also not the only (possibly or proven to be) unhealthy compounds often found in animal products—food is a package deal. Some other examples are saturated fat, trans fat, animal protein, heme-iron, bacterial endotoxins, heavy metals, persistent organic pollutants, pesticides/fungicides/herbicides, hormones, and antibiotics. That's not to let plants off the hook: some plants have some of those very same problems (e.g. arsenic in rice) as well as unique issues of individual species.

So yeah, pretty much anything we eat is unhealthy in some way. ;) Knowing that, it's probably a good idea to choose the least bad option and mostly eat things that are shown to be the least unhealthy—if one cares to lower one's risk of getting diseased early.
Namo tassa bhagavato arahato samma sambuddhassa
Namo tassa bhagavato arahato samma sambuddhassa
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SarathW
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Re: Why one meal a day?

Post by SarathW »

We eat food and the food eat us!
The best option may be to have variety of foods.
“As the lamp consumes oil, the path realises Nibbana”
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samseva
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Re: Why one meal a day?

Post by samseva »

Mkoll wrote:Oxidized cholesterol is also not the only (possibly or proven to be) unhealthy compounds often found in animal products—food is a package deal. Some other examples are saturated fat, trans fat, animal protein, heme-iron, bacterial endotoxins, heavy metals, persistent organic pollutants, pesticides/fungicides/herbicides, hormones, and antibiotics. That's not to let plants off the hook: some plants have some of those very same problems (e.g. arsenic in rice) as well as unique issues of individual species.

So yeah, pretty much anything we eat is unhealthy in some way. ;) Knowing that, it's probably a good idea to choose the least bad option and mostly eat things that are shown to be the least unhealthy—if one cares to lower one's risk of getting diseased early.
I agree (except for a few things like saturated fat, animal protein and heme iron :tongue: ). Contrary to what most think, food is not as pure and pristine as we think it is. When you look at a plate of your favourite dish, it is good to remember that it is probably filled with trace amounts of pesticides, heavy metals, chemicals and even a few bugs here and there. It develops asubha-saññā and the characteristic of dukkha, as well as reducing lust.
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Mkoll
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Re: Why one meal a day?

Post by Mkoll »

samseva wrote:
Mkoll wrote:Oxidized cholesterol is also not the only (possibly or proven to be) unhealthy compounds often found in animal products—food is a package deal. Some other examples are saturated fat, trans fat, animal protein, heme-iron, bacterial endotoxins, heavy metals, persistent organic pollutants, pesticides/fungicides/herbicides, hormones, and antibiotics. That's not to let plants off the hook: some plants have some of those very same problems (e.g. arsenic in rice) as well as unique issues of individual species.

So yeah, pretty much anything we eat is unhealthy in some way. ;) Knowing that, it's probably a good idea to choose the least bad option and mostly eat things that are shown to be the least unhealthy—if one cares to lower one's risk of getting diseased early.
I agree (except for a few things like saturated fat, animal protein and heme iron :tongue: ).
Here are a few studies about heme iron and its links to cancer and CVD and a few studies on animal protein and its links to obesity, IHD, and kidney stones(!). Animal protein is a bit harder to search for because there are so many results not relevant to human diet. The literature on saturated fat is voluminous so I won't bother quoting anything for now.

Meat and heme iron intake and esophageal adenocarcinoma in the European Prospective Investigation into Cancer and Nutrition study.
Abstract

Although recent studies suggest that high intakes of meat and heme iron are risk factors for several types of cancer, studies in relation to esophageal adenocarcinoma (EAC) are scarce. Previous results in the European Prospective Investigation into Cancer and Nutrition (EPIC) based on a relatively small number of cases suggested a positive association between processed meat and EAC. In this study, we investigate the association between intake of different types of meats and heme iron intake and EAC risk in a larger number of cases from EPIC. The study included 481,419 individuals and 137 incident cases of EAC that occurred during an average of 11 years of follow-up. Dietary intake of meat (unprocessed/processed red and white meat) was assessed by validated center-specific questionnaires. Heme iron was calculated as a type-specific percentage of the total iron content in meat. After adjusting for relevant confounders, we observed a statistically significant positive association of EAC risk with heme iron and processed meat intake, with HR: 1.67, 95% CI: 1.05-2.68 and HR: 2.27, 95% CI:1.33-3.89, respectively, for comparison of the highest vs. lowest tertile of intake. Our results suggest a potential association between higher intakes of processed meat and heme iron and risk of EAC.
Is heme iron intake associated with risk of coronary heart disease? A meta-analysis of prospective studies.
Abstract

PURPOSE:
Heme iron may contribute to the development of atherosclerosis by catalyzing production of hydroxyl-free radicals and promoting low-density lipoprotein oxidation. However, epidemiologic findings regarding the association between heme iron intake and risk of coronary heart disease (CHD) are inconsistent. We aimed to investigate the association by carrying out a meta-analysis of prospective studies.

METHODS:
Relevant studies were identified by using PubMed and EMBASE databases between January 1966 and April 2013 and also by manually reviewing the reference lists of retrieved publications. Summary relative risks (RRs) with corresponding 95% confidence intervals (CIs) were computed using a random-effects model.

RESULTS:
Six prospective studies, which contained a total of 131,553 participants and 2,459 CHD cases, met the inclusion criteria. Combined results indicated that participants with higher heme iron intake had a 31% increased risk of CHD, compared with those with lower intake (RR = 1.31, 95% CI 1.04-1.67), with significant heterogeneity (P(heterogeneity) = 0.05, I(2) = 55.0%). Excluding the only study from Japan (limiting to Western studies) yielded a RR of 1.46 (95% CI 1.21-1.76), with no study heterogeneity (P(heterogeneity) = 0.44, I(2) = 0.0%). The dose-response RR of CHD for an increase in heme iron intake of 1 mg/day was 1.27 (95% CI 1.10-1.47), with low heterogeneity (P (heterogeneity) = 0.25, I (2) = 25.8%). We observed no significant publication bias.

CONCLUSIONS:
This meta-analysis suggests that heme iron intake was associated with an increased risk of CHD.
A central role for heme iron in colon carcinogenesis associated with red meat intake.
Abstract
Epidemiology shows that red and processed meat intake is associated with an increased risk of colorectal cancer. Heme iron, heterocyclic amines, and endogenous N-nitroso compounds (NOC) are proposed to explain this effect, but their relative contribution is unknown. Our study aimed at determining, at nutritional doses, which is the main factor involved and proposing a mechanism of cancer promotion by red meat. The relative part of heme iron (1% in diet), heterocyclic amines (PhIP + MeIQx, 50 + 25 μg/kg in diet), and NOC (induced by NaNO₂+ NaNO₂; 0.17 + 0.23 g/L of drinking water) was determined by a factorial design and preneoplastic endpoints in chemically induced rats and validated on tumors in Min mice. The molecular mechanisms (genotoxicity, cytotoxicity) were analyzed in vitro in normal and Apc-deficient cell lines and confirmed on colon mucosa. Heme iron increased the number of preneoplastic lesions, but dietary heterocyclic amines and NOC had no effect on carcinogenesis in rats. Dietary hemoglobin increased tumor load in Min mice (control diet: 67 ± 39 mm²; 2.5% hemoglobin diet: 114 ± 47 mm², P = 0.004). In vitro, fecal water from rats given hemoglobin was rich in aldehydes and was cytotoxic to normal cells, but not to premalignant cells. The aldehydes 4-hydroxynonenal and 4-hydroxyhexenal were more toxic to normal versus mutated cells and were only genotoxic to normal cells. Genotoxicity was also observed in colon mucosa of mice given hemoglobin. These results highlight the role of heme iron in the promotion of colon cancer by red meat and suggest that heme iron could initiate carcinogenesis through lipid peroxidation.
Heme iron intake and acute myocardial infarction: a prospective study of men.
Abstract

BACKGROUND:
Epidemiologic studies of heme iron and non-heme iron intake in relation to risk of acute myocardial infarction (AMI) are lacking. Therefore, we examine the associations between heme iron and non-heme iron intake and fatal and nonfatal AMI in men. Moreover, we investigated whether the associations were modified by intake of minerals (calcium, magnesium, and zinc) that decreases iron absorption.

METHODS:
The population-based prospective cohort of Swedish Men (COSM) included 36882 men, aged 45-79 years, who completed a self-administered questionnaire on diet and had no history of coronary heart disease, stroke, diabetes, or cancer at baseline.

RESULTS:
During an 11.7 year follow-up, 678 fatal and 2593 nonfatal AMI events were registered. The hazard ratio (HR) of fatal AMI among men in the highest compared with the lowest quintile of heme iron intake was 1.51 (95%CI: 1.07-2.13, P-trend=0.02). The association was confined to men with a low intake of minerals that can decrease iron absorption. Among men with combined intakes of calcium, magnesium, and zinc below the medians, the HR of fatal AMI was 2.89 (95%CI: 1.43-5.82) for the highest vs. the lowest quintile of heme iron intake. There was no association between heme iron intake and nonfatal AMI, or between non-heme iron intake and fatal or nonfatal AMI.

CONCLUSIONS:
Findings from this prospective study indicate that a high heme iron intake, particularly with simultaneous low intake of minerals that can decrease iron absorption, may increase the risk of fatal AMI.
Dietary intake of heme iron and risk of cardiovascular disease: a dose-response meta-analysis of prospective cohort studies.
Abstract
BACKGROUND AND AIMS:
Iron is thought to play a fundamentally important role in the development of cardiovascular disease (CVD). This meta-analysis was performed to investigate the dose-response association between dietary intake of iron (including heme and non-heme iron) and the risk of CVD.

METHODS AND RESULTS:
We performed a search of the PubMed and Embase databases for prospective cohort studies of the association between dietary iron intake and CVD risk. Thirteen articles comprising 252,164 participants and 15,040 CVD cases were eligible for inclusion. Heme iron intake was associated significantly with increased risk of cardiovascular disease, and the pooled relative risk (RR) for each 1 mg/day increment was 1.07 (95% confidence interval: 1.01 to 1.14, I² = 59.7%). We also found evidence of a curvilinear association (P < 0.05 for non-linearity). In contrast, we found no association between CVD risk and dietary non-heme (0.98, 0.96 to 1.01, I² = 15.8%) or total iron (1.00, 0.94 to 1.06, I² = 30.4%). Subgroup analyses revealed that the association between heme iron intake and CVD risk was stronger among non-fatal cases (1.19, 1.07-1.33) and American patients (1.31, 1.11-1.56).

CONCLUSIONS:
Higher dietary intake of heme iron is associated with an increased risk of cardiovascular disease, whereas no association was found between CVD and non-heme iron intake or total iron intake. These findings may have important public health implications with respect to preventing cardiovascular disease.
Dietary protein and risk of ischemic heart disease in middle-aged men
ABSTRACT

Background: Prospective studies in US women have suggested an inverse relation between dietary protein and risk of ischemic heart disease (IHD). However, no large-scale prospective studies have been conducted in US men.

Objective: The objective was to examine the association between dietary protein and risk of IHD in a prospective study of US men. Design: Intakes of protein and other nutrients were assessed by using a validated food-frequency questionnaire at 4 time points during follow-up of 43,960 men participating in the Health Professionals Follow-Up Study. Cox proportional hazards models were used to calculate multivariable-adjusted relative risks (RRs) and 95% CIs.

Results: During 18 y of follow-up, we documented 2959 incident cases of IHD. The RR of IHD was 1.08 (95% CI: 0.95, 1.23; P for trend = 0.30) comparing the top with the bottom quintile of percentage of energy from total protein. RRs for animal and vegetable protein were 1.11 (95% CI: 0.97, 1.28; P for trend = 0.18) and 0.93
(95% CI: 0.78, 1.12; P for trend = 0.49), respectively. When the population was restricted to “healthy” men (those free of hypertension, hypercholesterolemia, and diabetes at baseline), the RR of IHD was 1.21 (95% CI: 1.01, 1.44; P for trend = 0.02) for total protein, 1.25 (95% CI: 1.04, 1.51; P for trend = 0.02) for animal protein, and 0.93 (95% CI: 0.72, 1.19; P for trend = 0.65) for vegetable protein.

Conclusions: We observed no association between dietary protein and risk of total IHD in this group of men aged 40–75 y. However, higher intake of animal protein may be associated with an increased risk of IHD in “healthy” men.
Animal protein and the risk of kidney stones: a comparative metabolic study of animal protein sources.
Abstract
PURPOSE:
We compared the effect of 3 animal protein sources on urinary stone risk.

MATERIALS AND METHODS:
A total of 15 healthy subjects completed a 3-phase randomized, crossover metabolic study. During each 1-week phase subjects consumed a standard metabolic diet containing beef, chicken or fish. Serum chemistry and 24-hour urine samples collected at the end of each phase were compared using mixed model repeated measures analysis.

RESULTS:
Serum and urinary uric acid were increased for each phase. Beef was associated with lower serum uric acid than chicken or fish (6.5 vs 7.0 and 7.3 mg/dl, respectively, each p <0.05). Fish was associated with higher urinary uric acid than beef or chicken (741 vs 638 and 641 mg per day, p = 0.003 and 0.04, respectively). No significant difference among phases was noted in urinary pH, sulfate, calcium, citrate, oxalate or sodium. Mean saturation index for calcium oxalate was highest for beef (2.48), although the difference attained significance only compared to chicken (1.67, p = 0.02) but not to fish (1.79, p = 0.08).

CONCLUSIONS:
Consuming animal protein is associated with increased serum and urine uric acid in healthy individuals. The higher purine content of fish compared to beef or chicken is reflected in higher 24-hour urinary uric acid. However, as reflected in the saturation index, the stone forming propensity is marginally higher for beef compared to fish or chicken. Stone formers should be advised to limit the intake of all animal proteins, including fish.
The potential impact of animal protein intake on global and abdominal obesity: evidence from the Observation of Cardiovascular Risk Factors in Luxembourg (ORISCAV-LUX) study.
OBJECTIVE:
To examine the association of total animal protein intake and protein derived from different dietary sources (meat; fish and shellfish; eggs; milk products) with global and abdominal obesity among adults in Luxembourg.

DESIGN:
Binary logistic regression analysis was used to assess the relationship between animal protein intake (as a percentage of total energy intake) and global obesity (BMI ≥ 30.0 kg/m(2)) and abdominal obesity (waist circumference ≥ 102 cm for men and ≥ 88 cm for women), after controlling for potential confounders.

SETTING:
Observation of Cardiovascular Risk Factors in Luxembourg (ORISCAV-LUX) study.

SUBJECTS:
The study population was derived from a national cross-sectional stratified sample of 1152 individuals aged 18-69 years, recruited between November 2007 and January 2009.

RESULTS:
There was an independent positive association between total animal protein intake and both global (OR = 1.18; 95% CI 1.12, 1.25) and abdominal obesity (OR = 1.14; 95% CI 1.08, 1.20) after adjustment for age, gender, education, smoking, physical activity and intakes of total fat, carbohydrate, fibre, and fruit and vegetables. Protein intakes from meat, fish and shellfish were positively associated with global and abdominal obesity with further adjustment for vegetal protein and other sources of animal-derived protein (all P < 0.01). Protein derived from eggs or milk products was unrelated to global or abdominal obesity.

CONCLUSIONS:
Our findings suggest that protein derived from animal sources, in particular from meat, fish and shellfish, may be associated with increased risk of both global and abdominal obesity among presumably healthy adults in Luxembourg. These findings suggest that lower animal protein intakes may be important for maintenance of healthy body weight.
Animal protein intake at 12 months is associated with growth factors at the age of six.
Abstract

AIM:
To study the associations between protein intake from different sources with anthropometry and serum insulin-like growth factor 1 (IGF-1) in infancy and childhood.

METHODS:
Children (n = 199) born in Iceland were followed up to six years of age. Their intake of various animal proteins and vegetable protein was calculated from weighed food records at 12 months and 6 years. Information about their weight and height at birth, 12 and 18 months, and 6 years was gathered. Serum IGF-1 was measured at 12 months and 6 years.

RESULTS:
At the age of six, children in the highest quartile for animal protein intake at 12 months (≥12.2% of total energy) had 0.8 kg/m(2) (95% CI = 0.1, 1.5) higher body mass index (BMI) than children in the lowest quartile (<7.6% of total energy). They were also heavier and longer in infancy and childhood. At 12 months, dairy protein intake as a percentage of total energy was associated with IGF-1 in six-year-old girls, β = 5.4 μg/L (95% CI = 2.5, 8.2).

CONCLUSION:
High animal protein intake in infancy, but not vegetable protein intake, was associated with accelerated growth and higher BMI in childhood. Dairy protein intake in infancy may be positively associated with linear growth and also with IGF-1 in six-year-old girls.
~~~
samseva wrote:Contrary to what most think, food is not as pure and pristine as we think it is. When you look at a plate of your favourite dish, it is good to remember that it is probably filled with trace amounts of pesticides, heavy metals, chemicals and even a few bugs here and there. It develops asubha-saññā and the characteristic of dukkha, as well as reducing lust.
That sounds like a helpful practice. Thanks for sharing.
Namo tassa bhagavato arahato samma sambuddhassa
Namo tassa bhagavato arahato samma sambuddhassa
Namo tassa bhagavato arahato samma sambuddhassa
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samseva
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Re: Why one meal a day?

Post by samseva »

Mkoll wrote:Here are a few studies about heme iron and its links to cancer and CVD and a few studies on animal protein and its links to obesity, IHD, and kidney stones(!). Animal protein is a bit harder to search for because there are so many results not relevant to human diet. The literature on saturated fat is voluminous so I won't bother quoting anything for now.

[…]

That sounds like a helpful practice. Thanks for sharing.
You're welcome, but for the rest, I'm kind of drained from discussing minute details of nutrition. Up to a point, it is basically ad infinitum and ad nauseam.
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Mkoll
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Re: Why one meal a day?

Post by Mkoll »

samseva wrote:
Mkoll wrote:Here are a few studies about heme iron and its links to cancer and CVD and a few studies on animal protein and its links to obesity, IHD, and kidney stones(!). Animal protein is a bit harder to search for because there are so many results not relevant to human diet. The literature on saturated fat is voluminous so I won't bother quoting anything for now.

[…]

That sounds like a helpful practice. Thanks for sharing.
You're welcome, but for the rest, I'm kind of drained from discussing minute details of nutrition. Up to a point, it is basically ad infinitum and ad nauseam.
Knowledge is power and the devil is in the details. ;)

But I do understand how one could have a sense of tedium with this.
Namo tassa bhagavato arahato samma sambuddhassa
Namo tassa bhagavato arahato samma sambuddhassa
Namo tassa bhagavato arahato samma sambuddhassa
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