Many diseases affect not only
humans but also some animal species. This leads to the conclusion that there
are similar proteins on the cell membranes and in the cytoplasm in humans and
animals. Digesting similar to our proteins may lead to an autoimmune reaction
against our proteins and degeneration of some tissues like blood endothelium,
respiratory endothelium cells, pancreas Langerhans cells, the cells of the
nephrons, or even the death or destruction of brain cells, causing great number
of diseases.
An Example for the
autoimmune theory is Diabetes Mellitus Type 1
Diabetes mellitus
type 1 has long been known medical disease. But lethality of diabetes begins
only when people begin to therapy it. Why?
It has long been
known that diabetes type 1 is caused by an immune response to beta cells of the
islets of Langerhans (of the same which go on vacation).
1. It is known that
the immune system responds only to proteins, i.e., Why not to the protein of
insulin?
2. It is known that
porcine insulin differs by only 2 amino acids from human. I.e. why not
exogenously induced immune response (e.g. alimentarian autoimmune reaction)?
The porcine insulin in the food gets into the gastro-intestinal tract, thence
through erosions of the gastrointestinal tract gets into the lymphatic system,
where antibodies against it are built. These antibodies react against porcine
insulin and against human insulin (because they are common in structure). Thus
they destroy the beta-cells of the islets of Langerhans by an immune reaction
type B. It leads to the conclusion that Type 1 diabetes is caused by
autoimmunity against insulin.
In conclusion: bovine
and porcine insulin are too common with human insulin. They are foreign protein
molecules and cause immune reaction, the antibodies built against them react
also to human insulin and cause the destruction of Beta-cells in pancreas,
inducing diabetes type I.
Another example of the logic of autoimmune theory is
Diabetes mellitus Type II
Bovine and porcine
receptors to insulin are also common with human receptors. Consuming big
amounts of them, found in the muscle tissue of animals, causes the production
of human antibodies against them. These antibodies connect themselves with
human insulin receptors in human organism. That causes insulin resistance in
human tissues. On back-forth connection mechanism this causes increasing of
insulin levels in blood. This causes constant hunger and increasing of food
consumption, thus obesity and metabolic syndrome. In this vicious circle soon
the capacity of human Langerhans cells to produce insulin is exhausted and this
leads to diabetes type II.
Obesity
is often associated with the development of insulin resistance. According to
the popular way to overcome insulin resistance, those affected should consume
meat and meat products and avoid carbohydrates that are rich in plants.
However, this is completely wrong. According to autoimmune theory, insulin
resistance and obesity are caused by eating meat with the food. Through food in
meat in the GIT enter a lot of animal insulin receptors (because muscle tissue
is rich with them) they pass through the intestinal wall into the interstitium
and in the lymph stream. These foreign proteins elicit an immune response and
the production of antibodies that mistakenly respond to the human insulin
receptors, causing insulin resistance and subsequent obesity and diabetes type
2. Therefore, the most appropriate treatment for obesity and diabetes is the
exclusion of animal products of food.
So perhaps in
Pandora`s box was nothing more than … some delicious pork steaks?
More evidence suggests type 2
diabetes is inflammatory disease
January 2, 2014
Source:
Federation of American Societies for Experimental
Biology
Summary:
As
people's waistlines increase, so does the incidence of type 2 diabetes. Now
scientists have a better understanding of exactly what happens in the body that
leads up to diabetes type 2, and what likely causes some of the complications
related to the disease. Specifically, scientists have found that in mice,
macrophages, a specific type of immune cell, invade the diabetic pancreatic
tissue during the early stages of the disease.
FULL STORY
As people's waistlines increase, so does the incidence
of type 2 diabetes. Now scientists have a better understanding of exactly what
happens in the body that leads up to diabetes type 2, and what likely causes
some of the complications related to the disease. Specifically, scientists from
Denmark have found that in mice, macrophages, a specific type of immune cell,
invade the diabetic pancreatic tissue during the early stages of the disease.
Then, these inflammatory cells produce a large amount of pro-inflammatory
proteins, called cytokines, which directly contribute to the elimination of
insulin-producing beta cells in the pancreas, resulting in diabetes. This
discovery was published in the January 2014 issue of the Journal of
Leukocyte Biology.
"The study may provide novel insights allowing
development of tailor-made anti-inflammatory based therapies reducing the
burden of type 2 patients," said Alexander Rosendahl, Ph.D., a researcher
involved in the work from the Department of Diabetes Complication Biology at
Novo Nordisk A/S, in Malov, Denmark. "These novel treatments may prove to
complement existing therapies such as insulin and GLP-1 analogues."
To make their discovery scientists compared obese mice
that spontaneously developed diabetes to healthy mice. The mice were followed
from a young age when the obese mice only showed early diabetes, to an age
where they displayed systemic complication in multiple organs. Presence of
macrophages around the beta cells in the pancreas and in the spleen was evaluated
by state-of-the-art flow cytometric technology allowing evaluation on a single
cell level. At both the early and late stages, the diabetic mice showed
significant modulations compared to healthy mice.
"The more researchers learn about obesity and
diabetes type 2, the more it appears that inflammation plays a critical role in
the progression and severity of these conditions," said John Wherry,
Ph.D., Deputy Editor of the Journal of Leukocyte Biology.
"This study sheds light on how a key inflammatory cell is connected to
disease and what might go wrong when someone has diabetes type 2. The knowledge
gained from such studies offers hope that new immune-based therapies could be
developed to mitigate the severity of such diseases."
Story Source:
Materials provided by Federation of
American Societies for Experimental Biology. Note: Content may be edited for style and
length.
Journal Reference:
1.
H. Cucak, L. G.
Grunnet, A. Rosendahl. Accumulation of M1-like macrophages in type 2
diabetic islets is followed by a systemic shift in macrophage polarization. Journal
of Leukocyte Biology, 2013; DOI: 10.1189/jlb.0213075
........................
The next articles makes us think if the wide
spread „therapy“ of diabetes with meat diet has any sense? It only proves that
there is some factor in meat that triggers the immune system, nothing else.
Meat Consumption as a Risk Factor for Type 2 Diabetes
Abstract
1. Introduction
Disease
risk factors identified in epidemiological studies serve as important public
health tools, helping clinicians identify individuals who may benefit from more
aggressive screening or risk-modification procedures, allowing policymakers to
prioritize intervention programs, and encouraging at-risk individuals to modify
behavior and improve their health. According to the American Diabetes
Association, the following factors justify testing for diabetes in asymptomatic
adults of any age with a body mass index ≥25 kg/m2 .
(1)Physical
inactivity
(2)First-degree
relative with diabetes
(3)High-risk
race/ethnicity (e.g., African American, Latino, Native American, Asian
American, Pacific Islander)
(4)Women
who delivered a baby weighing >9 lb or were diagnosed with gestational
diabetes
(5)Hypertension
(blood pressure ≥ 140/90 mmHg or on therapy for hypertension)
(6)High
density lipoprotein cholesterol level < 35 mg/dL (0.90 mmol/L) and/or a
triglyceride level > 250 mg/dL (2.82 mmol/L)
(7)Women
with polycystic ovarian syndrome
(8)A1C
≥ 5.7%, impaired glucose tolerance, or impaired fasting glucose on previous
testing
(9)Other
clinical conditions associated with insulin resistance (e.g., severe obesity,
acanthosis nigricans)
(10)History
of cardiovascular disease
Risk factors have
been based primarily on evidence from cross-sectional and prospective studies
(e.g., the association between obesity and type 2 diabetes) demonstrated in the
1976–1980 National Health and Nutrition Examination Survey [2]
and the association between ethnicity and diabetes described by the Centers for
Disease Control and Prevention, based on several data sets [3].
Most risk factors do not lend themselves to randomized trials.
The utility of
identifiable risk factors is illustrated by the link between excess body weight
and diabetes risk. In a combined report of data from the Nurses’ Health Study
and the Health Professionals Follow-up Study, men and women whose body mass
indices were in the overweight range (25.0 kg/m2–29.9 kg/m2)
were 4.6 and 3.5 times more likely to develop diabetes, respectively, compared
with those whose body mass indices were below 25 kg/m2 [4].
In the Diabetes Prevention Program, individuals in the placebo or lifestyle
treatment groups with body mass indices greater than 35 kg/m2 had
roughly double the risk of developing diabetes during the 3.2-year follow-up
period, compared with individuals with body mass indices below 30 kg/m2 [5].
As a result of these observations and similar findings in other studies,
clinicians are encouraged to screen all overweight and obese adults for
diabetes, rather than waiting to begin screening at age 45. In addition,
federal policies, including the Dietary Guidelines for Americans,
alert individuals regarding the risks of excess body weight.
While
some risk factors are not modifiable, eating habits are subject to change
through both individual action and broader policy initiatives. Although meat
consumption is an easily ascertained and commonly investigated variable
associated with diabetes risk, it has not yet been described as a diabetes risk
factor. In this article, we evaluate the evidence supporting the use of meat
consumption as a clinically useful risk factor for type 2 diabetes, based on
studies evaluating the risks associated with meat consumption as a categorical
dietary characteristic (i.e., meat consumption versus no
meat consumption), as a scalar variable (i.e., gradations of meat
consumption), or as part of a broader dietary pattern.
2. Findings
2.1. Risk Associated with Meat Consumption as a Categorical Variable
Researchers
investigating relationships between diet and disease risk have sought to
identify groups of individuals who differ on relevant dietary variables while
remaining reasonably homogeneous in other respects. In this regard, Seventh-day
Adventists have been an attractive population for study, because nearly all
Adventists avoid tobacco, alcohol, and caffeine, while roughly half are
omnivores and half are vegetarians, allowing researchers to identify the
effects of dietary variations in an otherwise health-conscious population.
Three large Adventist
cohorts have examined relationships between meat consumption and diabetes risk
in both cross-sectional and prospective analyses. The Adventist Mortality Study
included a baseline survey of 24,673 white Seventh-day Adventists living in
California in 1960, revealing 40% and 80% higher prevalence of diabetes among
meat-consuming women (prevalence ratio = 1.4, 95% CI, 1.2–1.8) and men
(prevalence ratio = 1.8, 95% CI, 1.3–2.5), respectively, compared with
vegetarians, after adjustment for age and body weight. Diabetes prevalence
increased as the frequency of meat consumption increased.
Published studies of the relationship between meat
consumption and risk of type 2 diabetes.
During the 21-year
follow-up of this cohort focusing on those who did not report diabetes at baseline,
the mention of diabetes on a death certificate was used as a surrogate for
diabetes prevalence. Compared with those who avoided meat, the relative risk of
having diabetes on a death certificate, adjusted for age, was 2.2 (RR = 2.2,
95% CI, 1.5–3.4) for meat-consuming men and 1.4 (RR = 1.4, 95% CI, 1.0–1.9) for
meat-consuming women. Meat consumption was defined as having red meat or
poultry at least once weekly (fish was reportedly rarely consumed in this
cohort). Further adjustment for body weight weakened these associations; the
increased risk remained significant for men, but not for women. Adjustment for
body mass index may lead to an underestimate of risk, as is discussed further
below.
The Adventist Health
Study included a baseline survey of 34,192 non-Hispanic white California
Adventists, showing that, age-adjusted, men and women who consumed meat had a
97% (OR = 1.97, 95% CI, 1.56–2.46, P = 0.0001) and 93% (OR =
1.93, 95% CI, 1.65–2.25, P = 0.0001) increased risk for
diabetes, respectively, compared with those who avoided meat.
In a 17-year
follow-up of 8401 individuals participating in either the Adventist Mortality
Study or the Adventist Health Study who were free of diabetes at baseline,
those who reported eating meat (defined as red meat, poultry, and fish) at
least weekly at the study’s endpoint were 29% more likely to have developed
diabetes, compared to those who reported no meat consumption at that time
point. Fish intake was uncommon in this cohort and, considered in isolation,
was associated with an increase in diabetes risk that did not reach statistical
significance (OR = 1.12, 95% CI, 0.88–1.44). Consumption of processed meats
(salted fish and frankfurters), adjusted for all other meat consumption, was
associated with a 27% increased risk of diabetes, compared with those who
avoided processed meats. Those who reported long-term meat consumption (i.e.,
intake at both the beginning and end of the study period) had a 74% increased
risk for developing diabetes, compared with those avoiding meat at both time
points. Adjustment for education, physical activity, smoking, and alcohol use
did not substantially alter the above findings. Adjustment for body mass index
or weight gain attenuated, but did not eliminate, the association between long-term
meat consumption and diabetes risk.
The Adventist Health
Study-2 included 60,903 Adventists, approximately one-quarter of whom were
black; most of the remainder were white. At baseline, diabetes prevalence was
3.2% among individuals consuming no meat, compared with 7.6% for those
consuming any sort of meat on a daily basis. Those consuming meat less than
weekly and those having no meat other than fish were between these extremes
(6.1% and 4.8%, respectively). After adjustment for body mass index, physical
activity, age, sex, ethnicity, and other factors, the odds ratio of a diagnosis
of type 2 diabetes among meat consumers remained approximately twice that of
individuals avoiding meat. Those who consumed meat less than once per week or
who limited their meat consumption to fish also remained at elevated risk,
albeit not so high as for those consuming all types of meat on a daily basis.
A
2-year follow-up period included 41,387 men and women. Compared with those
eating meat more than once per week and after adjustment for age, body mass
index, gender, ethnicity, income, and education, risk of developing diabetes
was significantly lower in vegans (odds ratio = 0.381, 95% CI, 0.236–0.617),
lacto-ovo-vegetarians (odds ratio = 0.618, 95% CI, 0.503–0.760), and those
consuming red meat or poultry less than once per week (odds ratio = 0.486, 95%
CI, 0.312–0.755). Risk was not significantly lower among those who ate fish but
no other meats (odds ratio = 0.790, 95% CI, 0.575–1.086). While the foregoing
studies indicate substantially increased risk of diabetes associated with meat
consumption independent of body weight, they do not settle the question as to
whether this association is mediated by the addition of meat per se or
by the displacement of plants that may follow the inclusion of meat in the
diet.
2.1.1. Risk Associated with Gradations of Meat Consumption
Among
meat-consuming populations, the contribution of gradations of meat consumption
to diabetes risk has been quantified in several prospective studies, both as an
isolated scalar variable and as part of a larger dietary pattern. A 2011
meta-analysis by Pan et al., including 442,101 participants and
28,228 diabetes cases, showed that consumption of both unprocessed and
processed red meat, as divided into quintiles, was significantly associated
with risk of type 2 diabetes. Processed meat was ascertained by questions about
use of “bacon”, “hot dogs” and “sausage, salami, bologna, and other processed
red meats” on a food frequency questionnaire. The relative risk associated per
100-g serving of unprocessed red meat per day was 1.19 (95% CI, 1.04–1.37). For
processed meat, the relative risk associated per 50-gram serving per day was
1.51 (95% CI, 1.25–1.83). The meta-analysis did not consider other types of
meat. In population studies that include a sufficient number people who avoid
all meats such that comparisons can be made between these people and those who
eat red meat, fish, etc., those who avoid all meats have the
lowest risks of diabetes. In studies, such as Pan’s, that examine gradations of
meat intake without a comparison to those who avoid meats altogether, red meat
and processed meat stand out as contributors to risk. This study confirmed the
results of two prior meta-analyses.
Among the data sets contributing
to this meta-analysis were two cohort studies that separated the risk
attributable to meat consumption per se from that related to
a more complex dietary pattern. In the Nurses’ Health Study I, two major
dietary patterns were identified among the 69,554 participants: a “Western”
dietary pattern, defined by higher intakes of red and processed meats, sweets,
and desserts, French fries, and refined grains, and a “prudent” dietary
pattern, characterized by higher intakes of fruits, vegetables, legumes, fish,
poultry, and whole grains [1].
After adjustment for age, family history of diabetes, calories, physical
activity, body mass index, and other factors, those in the highest quintile of
the Western pattern had a 49% (RR = 1.49, 95% CI 1.26–1.76, P <
0.001) increased risk of developing diabetes during 14 years of follow-up,
compared with those in the lowest quintile.
After adjustment for
the Western dietary score, the associations between meat intake and diabetes
risk remained significant; the relative risk for each added daily meat serving
was 1.26 (95% CI, 1.21–1.42) for red meat and 1.38 (95% CI, 1.23–1.56) for
processed meat, suggesting, in the study authors’ words, “that these foods are
associated with diabetes risk independently of the overall Western pattern”.
In the Nurses’ Health
Study II, including 91,246 women followed for eight years, consumption of
processed meat five or more times per week was associated with increased risk
of type 2 diabetes (RR = 1.91, 95% CI, 1.42–2.57, P <
0.001 for trend). Adjustment for a “Western” dietary pattern (associated with
higher intakes of red meat, processed meat, refined grain products, snacks,
sweets and desserts, French fries, and pizza) did not materially change this
result. For red meat consumption 5 or more times per week, compared with <1
time per week, in a multivariate model with further adjustment for a “Western”
dietary pattern, the relative risk of type 2 diabetes was 1.59 (95% CI,
1.01–2.49). These studies indicate that, while a Western dietary pattern is
associated with diabetes risk, meat consumption increases diabetes risk
independently of dietary pattern.
A separate analysis
examined fish consumption among 195,204 adults participating in the Nurses’
Health Study I, the Nurses’ Health Study II, or the Health Professionals
Follow-up Study. Those who consumed 5 or more fish servings per week had a 22%
increased risk (RR = 1.22, 95% CI, 1.08–1.39, P for trend
<0.001) for developing diabetes during the 14- to 18-year follow-up period,
compared with those who consumed fish less than once per month after adjustment
for body mass index, physical activity, family history of diabetes, caloric
intake, intakes of saturated and trans fats, and other
factors.
An additional and
methodologically distinct study examined diets of participants in the European
Prospective Investigation into Cancer and Nutrition Study and the Multiethnic
Cohort Study, finding that consumption of fish and meat was higher in
individuals with diabetes, compared with those without diabetes.
In
summary, these studies show that meat consumption is related to diabetes risk.
Available data do not exonerate any particular type of meat, and the role of
meat consumption in risk appears to be largely independent of its role as part
of a dietary pattern.
2.1.2. Mechanisms of Action
Although
the value of risk factors does not depend on the identification of mechanisms
by which they cause disease (as in the case of increased diabetes risk among
certain ethnic groups, for example), the presence of biological mechanisms
linking meat consumption with diabetes supports its validity as a bona
fide risk factor meriting the attention of clinicians and policymakers.
2.1.2.1. Effect on Body Weight
Nearly
all observational studies comparing meat-eaters with those who avoid meat show
higher body weights among the former group, a finding mirrored in the results
of intervention studies using meatless diets. The relatively high fat content
and the absence of fiber in meat products typically makes them higher in energy
density, compared with most vegetables, fruits, legumes, or grain products.
Dietary interventions omitting meat and other animal-derived products typically
lead to a reduction in energy intake without increased hunger. The reduction in
energy density is not fully compensated for by increased food intake. Recently
published findings from the Chicago Western Electric Study indicated an
association between animal protein intake and obesity, suggesting the
possibility of mechanisms influencing body weight other than those noted above.
The study authors proposed as possible explanatory mechanisms that insulin
resistance may be aggravated by the specific amino acids and fat that are
particularly abundant in meats and that saturated fatty acids in meat products
may increase the insulin response which, in turn, increases the respiratory
quotient and reduces fat oxidation.
While
low-carbohydrate diets that include meat often cause weight loss, this effect
is apparently not due to any special effect of meat consumption, but rather to
a reduction in energy intake that comes with the temporary exclusion of broad
categories of carbohydrate-containing foods.
To
the extent that meat’s contribution to overweight and obesity mediates its
tendency to increase diabetes risk, adjustment for body weight in studies of
diabetes risk is inappropriate and lead to an underestimate of the true degree
of risk. However, the tendency of meat consumption to increase body weight can
only partially explain the association with diabetes risk, because this
association is not fully attenuated after adjustment for body weight.
2.1.2.2. Effect on Visceral Fat
Apart
from the effect of generalized adiposity, it may be that visceral fat in
particular contributes to insulin resistance and risk of type 2 diabetes. A
diet eliminating meat was shown to reduce visceral fat and improve insulin
sensitivity, compared with a more conventional diabetic diet. A 2006 review
article by Hamdy and colleagues suggested that increased visceral adipose
tissue is associated with insulin resistance as a result of increased
proinflamatory cytokines originated from visceral fat cells and from adipose
tissue-resident macrophages.
2.1.2.3. Effect on Intracellular Lipid
Studies
have suggested that fat accumulation within muscle and liver cells (or the
metabolism of these lipids) aggravates insulin resistance which, in turn, contributes
to type 2 diabetes. Meat products are generally fattier than typical grains,
legumes, vegetables, and fruits. Nuts and seeds have a high fat content,
although lower in saturated fat than most meat products. Not only may dietary
fat contribute to intracellular lipid, but high-fat foods also appear to
downregulate the genes responsible for mitochondrial oxidative phosphorylation
in muscle tissue. Among individuals habitually avoiding animal products,
intramyocellular lipid concentrations were significantly lower, compared with
age- and weight-matched omnivores (−9.7, 95% CI −16.2 to −3.3, P =
0.01). These studies suggest that the inclusion of meat in the diet contributes
a load of dietary fat that enhances intracellular lipid storage and impairs
insulin metabolism which increases resistance. Indeed, nondiabetic individuals
following an omnivorous diet who then begin a diet omitting animal products
have demonstrated increased insulin sensitivity, although this may also reflect
the effect of weight loss and changes in intake of other food components.
2.1.2.4. Effect on Iron Balance
Meat
provides a substantial quantity of heme iron, which is more absorbable,
compared with non-heme iron. As a prooxidant, iron encourages the production of
reactive oxygen species, which may damage body tissues, including insulin-producing
pancreatic cells. Elevated body iron stores are associated with insulin
resistance, and even moderately elevated iron stores are associated with increased
risk for type 2 diabetes. Conversely, reductions in stored iron, through either
dietary changes or phlebotomy, increase insulin sensitivity. A 2009 review by
Liu and colleagues concluded that a reduction in heme iron intake would help
prevent insulin resistance, type 2 diabetes, and diabetes complications. In the
2011 meta-analysis cited above, intakes of red meat and of heme iron were
strongly correlated, and adjustment for heme iron intake attenuated the
relationship between red meat and diabetes risk.
2.1.2.5. Nitrates in Processed Meats
Processed
meats are similar to other meats in their macronutrient content, but may also
contain nitrites and sodium, both of which have been advanced as potential
explanations for the association between processed meats and diabetes.
2.1.2.6. Inflammation
Some
have speculated that that apparent deleterious effect of meat consumption on
glycemic control and diabetes risk is mediated by inflammation. A 2013 review
noted that meat-based diets, or “Western” dietary patterns, were positively
associated with biomarkers of inflammation, while fruit- and vegetable-based
diets, or “healthy” patterns, were inversely associated with biomarkers of
inflammation. Similarly, a 2014 Harvard study reported that as total red meat
consumption increased among women from the Nurses’ Health Study, so did biomarkers
of inflammation.
2.1.3. The Use of Risk Factors in Clinical Practice and Health Policies
Risk
factors for diabetes identified in research studies increase vigilance on the
part of clinicians, influence recommendations for screening, and encourage at-risk
individuals to modify their behavior. Risk factors related to diet can be
particularly useful. First, unlike family history, race, and even body weight,
they are readily modifiable. Second, they are linked not only to risk of
diabetes, but also to risk of cardiovascular disease, which is particularly
relevant to diabetes morbidity and mortality.
To put the degree of
risk in context, Hispanic ethnicity is associated with not quite twice the risk
for developing diabetes, compared with figures for non-Hispanic whites. Data
from the National Health Interview Survey (1984–2000) showed that, among males,
the lifetime risk at birth for developing diabetes was 45.4% for Hispanics,
compared with 26.7% for non-Hispanic whites. Among females, the figures were 52.5%
for Hispanics and 31.2% for non-Hispanic whites. Data from cross-sectional and
prospective studies suggest that individuals who regularly consume meat
products may have up to twice the risk of developing diabetes, compared with
individuals who avoid meat entirely.
Individuals who eat
meat regularly also tend to have higher plasma total and low density
lipoprotein cholesterol concentrations, higher blood pressure values, higher
risk of hypertension, and higher body weight, all of which contribute to cardiovascular
risk, the principal danger in diabetes. All of these conditions improve when
meat is no longer consumed. That is, lipid concentrations improve, due to the
reduction of saturated fatty acid and cholesterol intake and the increase in
soluble fiber and other plant constituents shown to alter plasma lipids; blood
pressure falls, due to the addition of components of plant foods (e.g.,
potassium) and the changing macronutrient content of the diet as evidenced by
the Dietary Approaches to Stop Hypertension (DASH) study, which was in part
inspired by observations of lower blood pressure among vegetarians; and body
weight diminishes, due to reduced energy density of the diet and, to a lesser
extent, increased post-prandial thermogenesis.
As we have noted, the
apparent problems of meat consumption are not limited to red meat. Although the
saturated fat load in poultry and fish products may be lower than in typical
red meats and omega-3 fatty acids account for a portion of the fat in many fish
species, saturated fat content is nonetheless generally higher in poultry and
fish than in typical vegetables, fruits, legumes, and grains. Poultry and fish
provide no fiber or complex carbohydrate and tend to displace foods that would
provide these nutrients, which may account for the differences in body weight
and in diabetes prevalence noted between fish-eaters and those who avoid all
meats. Per capita red meat consumption has fallen in the U.S. in recent
decades, while a compensatory increase in poultry and fish consumption has led
to overall increases in total per capita meat consumption.
Meat consumption as a
categorical variable is easily ascertainable by self-report. As such it is
clinically useful as a diabetes risk factor. While it is theoretically possible
to use dietary patterns or gradations of meat intake as risk factors, the
detailed dietary assessments that may be required to determine the degree of
risk are cumbersome in practice. Nonetheless, the fact that studies of
gradations of meat consumption indicate a dose-response relationship with
diabetes risk supports the validity of the use of meat consumption as a risk
factor.
Once identified,
at-risk individuals can be encouraged to familiarize themselves with meatless
options through recipes, cookbooks, online resources, and classes, and their
medical care-givers can enlist the expertise of dietetic professionals in
ensuring complete nutrition and providing group or individual instruction on
menu planning and related topics. In the research setting, plant-based dietetic
group instruction and support have helped at-risk individuals lose weight over
both the short and long term and improve insulin sensitivity.
Strengths
of the body of data contributing to this analysis include large sample sizes
and strong methodology in prospective studies, consistent findings among
studies, and a dose-response relationship. Limitations include the fact that
two of the cited Adventist cohorts were restricted to white participants.
However, confidence in the generalizability of these findings comes from
consistency with findings in non-Adventist populations. It is possible those
who abstain from meat also make other lifestyle choices that benefit health and
may in turn confound the findings of the reduced risk for type 2 diabetes. However,
the included studies have accounted for potential confounding factors to a
greater or lesser degree. Some reassurance derives from the use of stricter
controls in the more recent studies, which adjusted for age, smoking, calorie
and alcohol intake, and exercise, as well as in the similarity of results found
in clinical trials, including better glycemic control and reduced body weight.
While one may be tempted to combine data from the published studies in a
meta-analysis, the data sets and statistical procedures vary to the point that
such an analysis would be based on so many assumptions that it would not
enhance our understanding of the relationships under study.
3. Conclusions
Meat
consumption is consistently associated with diabetes risk. Dietary habits are
readily modifiable, but individuals and clinicians will consider dietary
changes only if they are aware of the potential benefits of doing so. The
foregoing review indicates that the identification of meat consumption as a
risk factor for diabetes provides helpful guidance for clinicians and at-risk
individuals, and sets the stage for beneficial behavioral changes.
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