Every great once in a while mainline medical advice reverses itself about something important – what was bad becomes good or what was good becomes bad. That happened with Vitamin D in recent years when stern warnings never to exceed 400IU a day gave way to recommendations that it is good for older people to take anywhere up to 4,000IU per day. A reversal may now be taking place having to do with whether nitrates and nitrites lead to cancers and Alzheimer’s Disease and are therefore bad for you, or whether they have great cardiovascular effects and are therefore good for you. There is controversy about this, clashing and clanging of gears as contradictory health advice is commonly given.
The issue at hand is whether it is good or bad for your health to consume foods containing high amount of nitrates and nitrites, foods like processed meats and certain supplements like beet root juice. The controversy extends to whether the large quantities of nitrates used in mass-scale agriculture constitutes a public health hazard because of contamination of public water supplies with nitrates. Is this good or bad for public health? This Part 1 blog entry presents the research case against consumption of nitrites and nitrites. A following Part 2 blog entry presents the research case in favor of consumption of nitrites and nitrites. I added some additional citations here on January 10, 2010.
Nitrates/nitrites and nitrosamines
A nitrate is a polyatomic ion with the molecular formula NO3 while nitrites are salts of nitrous acid (HNO2) containing the nitrite ion NO2. “Nitrates can be reduced to nitrites by certain microorganisms present in foods and in the gastrointestinal tract(ref).” “Sodium nitrite is used for the curing of meat because it prevents bacterial growth and, in a reaction with the meat’s myoglobin, gives the product a desirable dark red color. Because of the toxicity of nitrite (the lethal dose of nitrite for humans is about 22 mg per kg body weight(ref)), the maximum allowed nitrite concentration in meat products is 200 ppm. Under certain conditions, especially during cooking, nitrites in meat can react with degradation products of amino acids, forming nitrosamines, which are known carcinogens(ref)”
“Under certain conditions not yet fully understood, the natural breakdown products of proteins known as amines can combine with nitrites to form compounds known as nitrosamines. There are many different types of nitrosamines, most of which are known carcinogens in test animals(ref).” Cooking a meat containing nitrites may generate greater or fewer nitrosamines depending on how the cooking takes place. “Thus, well done or burned bacon probably is potentially more hazardous than less well done bacon. Bacon cooked by microwave has less nitrosamine than fried bacon(ref).”
“Nitrosamines are formed by a chemical reaction between nitrites or other proteins. Sodium nitrite is deliberately added to meat and fish to prevent toxin production; it is also used to preserve, color and flavor meats. Ground beef, cured meats and bacon in particular contain abundant amounts of amines due to their high protein content. Because of the significant levels of added nitrates and nitrites, nitrosamines are nearly always detectable in these foods. Nitrosamines are also easily generated under strong acid conditions, such as in the stomach, or at high temperatures associated with frying or flame broiling. Reducing sodium nitrite content reduces nitrosamine formation in foods. — Nitrosamines basically become highly reactive at the cellular level, which then alters gene expression and causes DNA damage(ref).”
“As established by the U.S. Department of Agriculture (USDA) in the Meat Inspection Regulations – the use of nitrites, nitrates, or combinations of them cannot result in more than 200 parts per million (ppm), calculated as sodium nitrite, in the finished product(ref).” People may have significant exposure to nitrites and nitrates from eating vegetable as well as from eating processed meats. Green lettuce, spinach, celery and beets tend to have the greatest concentrations of nitrites and concentrations can be particularly high due to excessive pre-harvest use of fertilizers.
The health case against consumption of nitrates and nitrites
The arguments against consumption of substantial amounts of nitrates and nitrites are both old and new and are fairly convincing:
· Nitrites are converted into nitrosamines under a number of conditions, and nitrosamines are known to be toxic or carcinogenic.
· Exposure to nitrates, nitrites and nitrosamines is correlated with higher incidences of Alzheimer’s Disease, Parkinson’s disease and diabetes.
· Consumption of foods containing large amounts of nitrates or nitrites lead to higher incidences of several cancers.
· Shorter telomere lengths, biomarkers of aging, are associated with consumption of processed meats containing nitrates/nitrites/nitrosamines, but not with consumption of unprocessed meats.
Nitrates/nitrites/nitrosamines and Alzheimer’s Disease, Parkinson’s disease and diabetes
Consumption of excess nitrates/nitrites/nitrosamines seems to play a role in creating or worsening these disease processes.
The professionally-worded title of this 2009 publication conceals a strong underlying message: Epidemilogical trends strongly suggest exposures as etiologic agents in the pathogenesis of sporadic Alzheimer’s disease, diabetes mellitus, and non-alcoholic steatohepatitis: “Nitrosamines mediate their mutagenic effects by causing DNA damage, oxidative stress, lipid peroxidation, and pro-inflammatory cytokine activation, which lead to increased cellular degeneration and death. However, the very same pathophysiological processes comprise the “unbuilding” blocks of aging and insulin-resistance diseases including, neurodegeneration, diabetes mellitus (DM), and non-alcoholic steatohepatitis (NASH). Previous studies demonstrated that experimental exposure to streptozotocin, a nitrosamine-related compound, causes NASH, and diabetes mellitus Types 1, 2 and 3 (Alzheimer (AD)-type neurodegeneration). Herein, we review evidence that the upwardly spiraling trends in mortality rates due to DM, AD, and Parkinson’s disease typify exposure rather than genetic-based disease models, and parallel the progressive increases in human exposure to nitrates, nitrites, and nitrosamines via processed/preserved foods. We propose that such chronic exposures have critical roles in the pathogenesis of our insulin resistance disease pandemic. Potential solutions include: 1) eliminating the use of nitrites in food; 2) reducing nitrate levels in fertilizer and water used to irrigate crops; and 3) employing safe and effective measures to detoxify food and water prior to human consumption. Future research efforts should focus on refining our ability to detect and monitor human exposures to nitrosamines and assess early evidence of nitrosamine-mediated tissue injury and insulin resistance.”
As further reported in a 2009 Science Daily article Nitrates May Be Environmental Trigger For Alzheimer’s, Diabetes And Parkinson’s Disease “A new study by researchers at Rhode Island Hospital have found a substantial link between increased levels of nitrates in our environment and food with increased deaths from diseases, including Alzheimer’s, diabetes mellitus and Parkinson’s. The study was published in the Journal of Alzheimer’s Disease. — Led by Suzanne de la Monte, MD, MPH, of Rhode Island Hospital, researchers studied the trends in mortality rates due to diseases that are associated with aging, such as diabetes, Alzheimer’s, Parkinson’s, diabetes and cerebrovascular disease, as well as HIV. They found strong parallels between age adjusted increases in death rate from Alzheimer’s, Parkinson’s, and diabetes and the progressive increases in human exposure to nitrates, nitrites and nitrosamines through processed and preserved foods as well as fertilizers. — De la Monte and the authors propose that the increase in exposure plays a critical role in the cause, development and effects of the pandemic of these insulin-resistant diseases. — De la Monte — says, “We have become a ‘nitrosamine generation.’ In essence, we have moved to a diet that is rich in amines and nitrates, which lead to increased nitrosamine production. We receive increased exposure through the abundant use of nitrate-containing fertilizers for agriculture.” She continues, “Not only do we consume them in processed foods, but they get into our food supply by leeching from the soil and contaminating water supplies used for crop irrigation, food processing and drinking.” — Nitrites and nitrates belong to a class of chemical compounds that have been found to be harmful to humans and animals. More than 90 percent of these compounds that have been tested have been determined to be carcinogenic in various organs. They are found in many food products, including fried bacon, cured meats and cheese products as well as beer and water. Exposure also occurs through manufacturing and processing of rubber and latex products, as well as fertilizers, pesticides and cosmetics. – The researchers note that the role of nitrosamines has been well-studied, and their role as a carcinogen has been fully documented. The investigators propose that the cellular alterations that occur as a result of nitrosamine exposure are fundamentally similar to those that occur with aging, as well as Alzheimer’s, Parkinson’s and Type 2 diabetes mellitus. — De la Monte comments, “All of these diseases are associated with increased insulin resistance and DNA damage. Their prevalence rates have all increased radically over the past several decades and show no sign of plateau. Because there has been a relatively short time interval associated with the dramatic shift in disease incidence and prevalence rates, we believe this is due to exposure-related rather than genetic etiologies.”
A 2009 publication reinforces the message, at least insofar as nitrosamines are concerned, Nitrosamine exposure causes insulin resistance diseases: relevance to type 2 diabetes mellitus, non-alcoholic steatohepatitis, and Alzheimer’s disease. “The current epidemics of type 2 diabetes mellitus (T2DM), non-alcoholic steatohepatitis (NASH), and Alzheimer’s disease (AD) all represent insulin-resistance diseases. Previous studies showed that streptozotocin, a nitrosamine-related com-pound, causes insulin resistance diseases including, T2DM, NASH, and AD-type neurodegeneration. We hypothesize that chronic human exposure to nitrosamine compounds, which are widely present in processed foods, contributes to the pathogenesis of T2DM, NASH, and AD. Long Evans rat pups were treated with N-nitrosodiethylamine (NDEA) by i.p. (x3) or i.c. (x1) injection, and 2-4 weeks later, they were evaluated for cognitive-motor dysfunction, insulin resistance, and neurodegeneration using behavioral, biochemical, and molecular approaches. NDEA treatment caused T2DM, NASH, deficits in motor function and spatial learning, and neurodegeneration characterized by insulin resistance and deficiency, lipid peroxidation, cell loss, increased levels of amyloid-beta protein precursor/amyloid-beta, phospho-tau, and ubiquitin immunoreactivities, and upregulated expression of pro-inflammatory cytokine and pro-ceramide genes, which together promote insulin resistance. In conclusion, environmental and food contaminant exposures to nitrosamines play critical roles in the pathogenesis of major insulin resistance diseases including T2DM, NASH, and AD. Improved detection and prevention of human exposures to nitrosamines will lead to earlier treatments and eventual quelling of these costly and devastating epidemics.”
Another 2009 publication continues the theme Mechanisms of nitrosamine-mediated neurodegeneration: potential relevance to sporadic Alzheimer’s disease. “Streptozotocin (STZ) is a nitrosamine-related compound that causes Alzheimer’s disease (AD)-type neurodegeneration with cognitive impairment, brain insulin resistance, and brain insulin deficiency. Nitrosamines and STZ mediate their adverse effects by causing DNA damage, oxidative stress, lipid peroxidation, pro-inflammatory cytokine activation, and cell death, all of which occur in AD. We tested the hypothesis that exposure to N-nitrosodiethylamine (NDEA), which is widely present in processed/preserved foods, causes AD-type molecular and biochemical abnormalities in central nervous system (CNS) neurons. NDEA treatment of cultured post-mitotic rat CNS neurons (48 h) produced dose-dependent impairments in ATP production and mitochondrial function, and increased levels of 8-hydroxy-2′-deoxyguanosine, 4-hydroxy-2-nonenal, phospho-tau, amyloid-beta protein precursor-amyloid-beta (A beta PP-A beta), and ubiquitin immunoreactivity. These effects were associated with decreased expression of insulin, insulin-like growth factor (IGF)-I, and IGF-II receptors, and choline acetyltransferase. Nitrosamine exposure causes neurodegeneration with a number of molecular and biochemical features of AD including impairments in energy metabolism, insulin/IGF signaling mechanisms, and acetylcholine homeostasis, together with increased levels of oxidative stress, DNA damage, and A beta PP-A beta immunoreactivity. These results suggest that environmental exposures and food contaminants may play critical roles in the pathogenesis of sporadic AD.”
Nitrates, nitrites and nitrosamines and cancer
The 2008 publication Processed meat and colorectal cancer: a review of epidemiologic and experimental evidence implicates nitrites and nitrosamines “Processed meat intake may be involved in the etiology of colorectal cancer, a major cause of death in affluent countries. The epidemiologic studies published to date conclude that the excess risk in the highest category of processed meat-eaters is comprised between 20% and 50% compared with non-eaters. In addition, the excess risk per gram of intake is clearly higher than that of fresh red meat. Several hypotheses, which are mainly based on studies carried out on red meat, may explain why processed meat intake is linked to cancer risk. Those that have been tested experimentally are (i) that high-fat diets could promote carcinogenesis via insulin resistance or fecal bile acids; (ii) that cooking meat at a high temperature forms carcinogenic heterocyclic amines and polycyclic aromatic hydrocarbons; (iii) that carcinogenic N-nitroso compounds are formed in meat and endogenously; (iv) that heme iron in red meat can promote carcinogenesis because it increases cell proliferation in the mucosa, through lipoperoxidation and/or cytotoxicity of fecal water. Nitrosation might increase the toxicity of heme in cured products.”
The 2008 publication Nutrition and gastric cancer risk: an update relates “Data from epidemiologic, experimental, and animal studies indicate that diet plays an important role in the etiology of gastric cancer. High intake of fresh fruits and vegetables, lycopene and lycopene-containing food products, and potentially vitamin C and selenium may reduce the risk for gastric cancer. Data also suggest that high intake of nitrosamines, processed meat products, salt and salted foods, and overweight and obesity are associated with increased risk for gastric cancer. However, current data provide little support for an association of beta-carotene, vitamin E, and alcohol consumption with risk for gastric cancer.”
The 2010 publication Nitrate intake and the risk of thyroid cancer and thyroid disease relates “BACKGROUND: Nitrate is a contaminant of drinking water in agricultural areas and is found at high levels in some vegetables. Nitrate competes with uptake of iodide by the thyroid, thus potentially affecting thyroid function.– METHODS: We investigated the association of nitrate intake from public water supplies and diet with the risk of thyroid cancer and self-reported hypothyroidism and hyperthyroidism in a cohort of 21,977 older women in Iowa who were enrolled in 1986 and who had used the same water supply for >10 years. — We observed no association with prevalence of hypothyroidism or hyperthyroidism. Increasing intake of dietary nitrate was associated with an increased risk of thyroid cancer (highest vs. lowest quartile, RR = 2.9 [1.0-8.1]; P for trend = 0.046) and with the prevalence of hypothyroidism (odds ratio = 1.2 [95% CI = 1.1-1.4]), but not hyperthyroidism. – CONCLUSIONS: Nitrate may play a role in the etiology of thyroid cancer and warrants further study.”
The 2007 report Nitrate intake relative to antioxidant vitamin intake affects gastric cancer risk: a case-control study in Korea had some surprising conclusions: “The objective of this study was to determine whether the intake of nitrate relative to antioxidant vitamin rather than absolute intake of nitrate affects the risk of gastric cancer (GC). In a case-control study in Korea using a food frequency questionnaire, trained dietitians interviewed 136 GC cases and an equal number of controls matched by sex and age. As an index of nitrate intake relative to antioxidant vitamins intake, we calculated the nitrate:antioxidant vitamin consumption ratio. The mean daily nitrate intake from foods was very high in our subjects. Higher absolute intake of nitrate was not associated with GC risk [odds ratios (OR) = 1.13; 95% confidence interval (CI) = 0.42-3.06]. However, the GC risk distinctly increased as the nitrate:antioxidant vitamin consumption ratio increased, particularly with higher nitrate:vitamin E (OR = 2.78; 95% CI = 1.01-7.67) and nitrate:folate ratios (OR = 3.37; 95% CI = 1.28-8.87). Therefore, GC risk was influenced by the intake of nitrate relative to antioxidant vitamins. Our results suggest that a decrease in the intake of nitrate relative to antioxidant vitamins is considerably more effective in reducing GC risk than either a lower absolute intake of nitrate or a higher intake of antioxidant vitamins alone.”
Note that there is a theme here that shows up frequently in the literature: cancer and other risks associated with ingestion of nitrites or nitrites or nitrosamines can be reduced by consumption of antioxidants.
A number of other recent publications link nitric oxide to cancers. The 2007 publication An emerging role for endothelial nitric oxide synthase in chronic inflammation and cancer relates “Nitric oxide (NO) is a free radical that is involved in carcinogenesis. Recent literature indicates that endothelial NO synthase (eNOS) can modulate cancer-related events (angiogenesis, apoptosis, cell cycle, invasion, and metastasis). We review the literature linking eNOS to carcinogenesis to encourage future research assessing the role of eNOS in cancer prevention and treatment.”
The 2010 publication Nitric oxide and cancer relates “Nitric oxide (NO) is a lipophilic, highly diffusible and short-lived physiological messenger which regulates a variety of important physiological responses including vasodilation, respiration, cell migration, immune response and apoptosis. NO is synthesized by three differentially gene-encoded NO synthase (NOS) in mammals: neuronal NOS (nNOS or NOS-1), inducible NOS (iNOS or NOS-2) and endothelial NOS (eNOS or NOS-3). All isoforms of NOS catalyze the reaction of L-arginine, NADPH and oxygen to NO, L-citrulline and NADP. NO may exert its cellular action by cGMP-dependent as well as by cGMP-independent pathways including postranslational modifications in cysteine (S-nitrosylation or S-nitrosation) and tyrosine (nitration) residues, mixed disulfide formation (S-nitrosoglutathione or GSNO) or promoting further oxidation protein stages which have been related to altered protein function and gene transcription, genotoxic lesions, alteration of cell-cycle check points, apoptosis and DNA repair. NO sensitizes tumor cells to chemotherapeutic compounds. The expression of NOS-2 and NOS-3 has been found to be increased in a variety of human cancers. The multiple actions of NO in the tumor environment is related to heterogeneous cell responses with particular attention in the regulation of the stress response mediated by the hypoxia inducible factor-1 and p53 generally leading to growth arrest, apoptosis or adaptation.” Several earlier publications also link NO to cancers, for example the 2003 publication Nitric oxide-mediated promotion of mammary tumour cell migration requires sequential activation of nitric oxide synthase, guanylate cyclase and mitogen-activated protein kinase. “ Together, these results indicate sequential activation of NOS, GC and MAPK pathways in mediating signals for C3L5 cell migration, an essential step in invasion and metastasis. Since NOS activity is positively associated with human breast cancer progression, the present results are relevant for development of therapeutic modalities for this disease.”
The 2009 publication Dietary intake of polyphenols, nitrate and nitrite and gastric cancer risk in Mexico City reports: “N-nitroso compounds (NOC) are potent animal carcinogens and potential human carcinogens. The primary source of exposure for most individuals may be endogenous formation, a process that can be inhibited by dietary polyphenols. To estimate the risk of gastric cancer (GC) in relation to the individual and combined consumption of polyphenols and NOC precursors (nitrate and nitrite), a population-based case-control study was carried out in Mexico City from 2004 to 2005 including 257 histologically confirmed GC cases and 478 controls. Intake of polyphenols, nitrate and nitrite were estimated using a food frequency questionnaire. High intakes of cinnamic acids, secoisolariciresinol and coumestrol were associated with an approximately 50% reduction in GC risk. A high intake of total nitrite as well as nitrate and nitrite from animal sources doubled the GC risk. Odds ratios around 2-fold were observed among individuals with both low intake of cinnamic acids, secoisolariciresinol or coumestrol and high intake of animal-derived nitrate or nitrite, compared to high intake of the polyphenols and low animal nitrate or nitrite intake, respectively. Results were similar for both the intestinal and diffuse types of GC. Our results show, for the first time, a protective effect for GC because of higher intake of cinnamic acids, secoisolariciresinol and coumestrol, and suggest that these polyphenols reduce GC risk through inhibition of endogenous nitrosation. The main sources of these polyphenols were pears, mangos and beans for cinnamic acids; beans, carrots and squash for secoisolariciresinol and legumes for coumestrol.”
The 2008 publication Geographic distribution of liver and stomach cancers in Thailand in relation to estimated dietary intake of nitrate, nitrite, and nitrosodimethylamine reports “It is our working hypothesis that the high rate of the liver and gastric cancers in North and Northeast Thailand is associated with increased daily dietary intake of nitrate, nitrite, and nitrosodimethylamine (NDMA).– Significant differences in dietary nitrate, nitrite, and NDMA intakes were seen between various Thai regions (P < 0.0001), and these corresponded to the variations in liver and stomach cancer ASR values between the regions. –”
Going back to 2001 we have the publication Municipal drinking water nitrate level and cancer risk in older women: the Iowa Women’s Health Study. This study was based on a cohort of 21,977 Iowa women who were 55-69 years of age at baseline in 1986 and had used the same water supply more than 10 years. The study showed a positive association with increasing nitrate in drinking water with bladder cancer but not for other cancers.
The 2009 publication Too much of a good thing? Nitrate from nitrogen fertilizers and cancer points to a possible public health problem. “Nitrate levels in water supplies have been increasing in many areas of the world; therefore, additional studies of populations with well-characterized exposures are urgently needed to further our understanding of cancer risk associated with nitrate ingestion. Future studies should assess exposure for individuals (e.g., case-control, cohort studies) in a time frame relevant to disease development, and evaluate factors affecting nitrosation. Estimating N-nitroso compounds formation via nitrate ingestion requires information on dietary and drinking water sources of nitrate, inhibitors of nitrosation (e.g., vitamin C), nitrosation precursors (e.g., red meat, nitrosatable drugs), and medical conditions that may increase nitrosation (e.g., inflammatory bowel disease). Studies should account for the potentially different effects of dietary and water sources of nitrate and should include the population using private wells for whom exposure levels are often higher than public supplies.”
The 2010 study Estimation of incidence and social cost of colon cancer due to nitrate in drinking water in the EU: a tentative cost-benefit assessment concludes “RESULTS: For above median meat consumption the risk of colon cancer doubles when exposed to drinking water exceeding 25 mg/L of nitrate (NO3) for more than ten years. — CONCLUSIONS: Our cost estimates indicate that current measures to prevent exceedance of 50 mg/L NO3 are probably beneficial for society and that a stricter nitrate limit and additional measures may be justified. –”
Eating processed meat and telomere lengths
The blog entry Telomere lengths, Part 2: Lifestyle, dietary, and other factors associated with telomere shortening and lengthening contains a long passage related to the different impacts of eating processed meats and unprocessed meats on telomere lengths. Because the difference between processed and unprocessed meats is largely associated with inclusion of nitrates/nitrites and nitrosamines, the passage is worth reproducing here:
Telomere lengths and processed meats
It is possible to couple the results of two studies related to processed meats to see some interesting relationships. The first such study is described in a 2010 publication published in Circulation, a journal of the American Heart Association Red and Processed Meat Consumption and Risk of Incident Coronary Heart Disease, Stroke, and Diabetes Mellitus. This study is a meta-analysis of studies relating red and processed meat to CHD (coronary heart disease), stroke, and diabetes mellitus. “Background— Meat consumption is inconsistently associated with development of coronary heart disease (CHD), stroke, and diabetes mellitus, limiting quantitative recommendations for consumption levels. Effects of meat intake on these different outcomes, as well as of red versus processed meat, may also vary. — Methods and Results— We performed a systematic review and meta-analysis of evidence for relationships of red (unprocessed), processed, and total meat consumption with incident CHD, stroke, and diabetes mellitus. We searched for any cohort study, case-control study, or randomized trial that assessed these exposures and outcomes in generally healthy adults. Of 1598 identified abstracts, 20 studies met inclusion criteria, including 17 prospective cohorts and 3 case-control studies. All data were abstracted independently in duplicate. Random-effects generalized least squares models for trend estimation were used to derive pooled dose-response estimates. The 20 studies included 1 218 380 individuals and 23 889 CHD, 2280 stroke, and 10 797 diabetes mellitus cases. Red meat intake was not associated with CHD (n=4 studies; relative risk per 100-g serving per day=1.00; 95% confidence interval, 0.81 to 1.23; P for heterogeneity=0.36) or diabetes mellitus (n=5; relative risk=1.16; 95% confidence interval, 0.92 to 1.46; P=0.25). Conversely, processed meat intake was associated with 42% higher risk of CHD (n=5; relative risk per 50-g serving per day=1.42; 95% confidence interval, 1.07 to 1.89; P=0.04) and 19% higher risk of diabetes mellitus (n=7; relative risk=1.19; 95% confidence interval, 1.11 to 1.27; P<0.001). Associations were intermediate for total meat intake. Consumption of red and processed meat were not associated with stroke, but only 3 studies evaluated these relationships. — Conclusions— Consumption of processed meats, but not red meats, is associated with higher incidence of CHD and diabetes mellitus. These results highlight the need for better understanding of potential mechanisms of effects and for particular focus on processed meats for dietary and policy recommendations.”
The second study (2008) looks at telomere lengths as related to kinds of food intake Dietary patterns, food groups, and telomere length in the Multi-Ethnic Study of Atherosclerosis (MESA). “Objective: With data from 840 white, black, and Hispanic adults from the Multi-Ethnic Study of Atherosclerosis, we studied cross-sectional associations between telomere length and dietary patterns and foods and beverages that were associated with markers of inflammation. — Design: Leukocyte telomere length was measured by quantitative polymerase chain reaction. Length was calculated as the amount of telomeric DNA (T) divided by the amount of a single-copy control DNA (S) (T/S ratio). Intake of whole grains, fruit and vegetables, low-fat dairy, nuts or seeds, nonfried fish, coffee, refined grains, fried foods, red meat, processed meat, and sugar-sweetened soda were computed with responses to a 120-item food-frequency questionnaire completed at baseline. Scores on 2 previously defined empirical dietary patterns were also computed for each participant. Results: After adjustment for age, other demographics, lifestyle factors, and intakes of other foods or beverages, only processed meat intake was associated with telomere length. For every 1 serving/d greater intake of processed meat, the T/S ratio was 0.07 smaller (Î² ± SE: –0.07 ± 0.03, P = 0.006). Categorical analysis showed that participants consuming 1 serving of processed meat each week had 0.017 smaller T/S ratios than did nonconsumers. Other foods or beverages and the 2 dietary patterns were not associated with telomere length. – Conclusions: Processed meat intake showed an expected inverse association with telomere length, but other diet features did not show their expected associations.
So, together the two studies say:
· Consumption of processed meat correlates with both shorter telomere lengths and increased susceptibility to CHD and diabetes mellitus. Neither of these correlations exist for consumption of red meat.
· Of a number of possibly not-good-for-you foods like sugar-sweetened soda, only consumption of processed meats was correlated with shorter telomeres.
· Causal chain is unclear, e.g. whether eating processed meats leads to shorter telomeres which leads to increased disease susceptibilities or whether eating processed meats leads to disease susceptibilities which lead to shorter telomeres, or both or neither.
From a health and longevity perspective the two studies combine fairly powerfully to contraindicate eating processed meats, foods which have long been suspected to be carcinogenic because they tend to be infused with nitrites(ref).
I resist the temptation to go on quoting more and more publications that are negative about nitrates/nitrites/nitrosamines. A few central points seem to be made:
1. A number of both laboratory and epidemiological studies suggest strong associations between consumption of nitrates/nitrites/nitrosamines with many diseases including Alzheimer’s disease, Parkinson’s disease, diabetes and multiple cancers. The chain of causality is fairly well understood in terms of actions of nitrates/nitrites/nitrosamines.
2. Telomere lengths, a proxy measure for aging, are definitely shorter among those eating processed meat but not unprocessed meat, again implicating nitrates/nitrites/nitrosamines. Likewise eating processed meat but not unprocessed meat is associated with greater susceptibility to coronary heart disease and diabetes mellitus.
3. The major sources of nitrates/nitrites/nitrosamines are drinking water contaminated with fertilizer runoff, certain vegetables and processed meat.
4. The health risks associated with consumption of nitrates/nitrites/nitrosamines can be significantly reduced by consumption of antioxidants and plant-based polyphenols which interfere with nitrosation.
One would think that with the collective evidence presented above, no respectable health scientists would advocate consuming nitrates or nitrites for health reasons. However, in the past few years a case is being built up for exactly that. In fact certain health supplements like beet root juice are being sold precisely because they are concentrated sources of nitrates. The case for nitrates/nitrites seems to be that they lead to increased nitric oxide expression in the body and offer a number of positive cardiovascular benefits. I will present this case in the following blog entry Nitrates and nitrites –Part 2: good for you.