Jay Sosa said:
It was just some pic I took from google, I sure as hell don't put sugar in my cereal.
And I always was under the impression that you should not eat too much meat no matter if organic or lean or whatever. May I ask where you guys get your vitamines and fibers from? Please con't tell me from pills..
Maybe we should differentiate between eating just to lose weight and eating healthy and losing weight. Eating red meat every day is NOT healthy.
Too much meat? The Eskimos & Inuit ate almost entirely meat and were documented as being very healthy and living to an old age.
Give me controlled studies showing that red meat is bad. I don't want government guidelines, tabloid 'science' articles like from msnbc/cnn.com, but links to studies.
I'll give you something to start with, which is what I linked you to in whole health source, but since you clearly didn't read it, I'll post the abstracts/conclusions.
Vitamin K2 & CLA from red meat and dairy:
BACKGROUND AND AIM: Vitamin K dependent proteins have been demonstrated to inhibit vascular calcification. Data on the effect of vitamin K intake on coronary heart disease (CHD) risk, however, are scarce. To examine the relationship between dietary vitamins K(1) and K(2) intake, and its subtypes, and the incidence of CHD. METHODS AND RESULTS: We used data from the Prospect-EPIC cohort consisting of 16,057 women, enrolled between 1993 and 1997 and aged 49-70 years, who were free of cardiovascular diseases at baseline. Intake of vitamin K and other nutrients was estimated with a food frequency questionnaire. Multivariate Cox proportional hazards models were used to analyse the data. After a mean+/-SD follow-up of 8.1+/-1.6 years, we identified 480 incident cases of CHD. Mean vitamin K(1) intake was 211.7+/-100.3 microg/d and vitamin K(2) intake was 29.1+/-12.8 microg/d. After adjustment for traditional risk factors and dietary factors, we observed an inverse association between vitamin K(2) and risk of CHD with a Hazard Ratio (HR) of 0.91 [95% CI 0.85-1.00] per 10 microg/d vitamin K(2) intake. This association was mainly due to vitamin K(2) subtypes MK-7, MK-8 and MK-9. Vitamin K(1) intake was not significantly related to CHD. CONCLUSIONS: A high intake of menoquinones, especially MK-7, MK-8 and MK-9, could protect against CHD. However, more research is necessary to define optimal intake levels of vitamin K intake for the prevention of CHD.
http://www.ncbi.nlm.nih.gov/pubmed/19179058
BACKGROUND: Despite the high saturated fat content of dairy products, no clear association between dairy product intake and risk of myocardial infarction (MI) has been observed. Dairy products are the main source of conjugated linoleic acid (CLA; 18:2n-7t), which is produced by the ruminal biohydrogenation of grasses eaten by cows. Pasture-grazing dairy cows have more CLA in their milk than do grain-fed cows. Some animal models have reported beneficial effects of CLA on atherosclerosis. OBJECTIVE: The objective was to determine the association between the 9c,11t-CLA isomer in adipose tissue and risk of MI. DESIGN: The studied population consisted of 1813 incident cases of a first nonfatal acute MI and 1813 population-based controls matched for age, sex, and area of residence. All subjects lived in Costa Rica-a country that uses traditional pasture-grazing for dairy cows. Conditional logistic regression was used to estimate multivariate odds ratios and 95% CIs. RESULTS: Adipose tissue 9c,11t-CLA was associated with a lower risk of MI in basic and multivariate models. Compared with the lowest quintile, odds ratios and 95% CIs were 0.80 (0.61, 1.04) for the second, 0.86 (0.64, 1.14) for the third, 0.62 (0.46, 0.84) for the fourth, and 0.51 (0.36, 0.71) for the fifth quintiles (P for trend <0.0001). Dairy intake was not associated with risk of MI, despite a strong risk associated with saturated fat intake. CONCLUSION: 9c,11t-CLA, which is present in meaningful amounts in the milk of pasture-grazed cows, might offset the adverse effect of the saturated fat content of dairy products.
http://www.ncbi.nlm.nih.gov/pubmed/20463040
BACKGROUND: Anticarcinogenic activities of vitamin K have been observed in animal and cell studies. OBJECTIVE: On the basis of the growth inhibitory effects of vitamin K as observed in a variety of cancer cell lines, we hypothesized that dietary intake of phylloquinone (vitamin K(1)) and menaquinones (vitamin K(2)) may be associated with overall cancer incidence and mortality. DESIGN: In the prospective EPIC-Heidelberg (European Prospective Investigation into Cancer and Nutrition-Heidelberg) cohort study, 24,340 participants aged 35-64 y and free of cancer at enrollment (1994-1998) were actively followed up for cancer incidence and mortality through 2008. Dietary vitamin K intake was estimated from food-frequency questionnaires completed at baseline by using HPLC-based food-composition data. Multivariate-adjusted hazard ratios (HRs) and 95% CIs were estimated by using Cox proportional hazards models. RESULTS: During a median follow-up time of >10 y, 1755 incident cancer cases occurred, of which 458 were fatal. Dietary intake of menaquinones was nonsignificantly inversely associated with overall cancer incidence (HR for the highest compared with the lowest quartile: 0.86; 95% CI: 0.73, 1.01; P for trend = 0.08), and the association was stronger for cancer mortality (HR: 0.72; 95% CI: 0.53, 0.98; P for trend = 0.03). Cancer risk reduction with increasing intake of menaquinones was more pronounced in men than in women, mainly driven by significant inverse associations with prostate (P for trend = 0.03) and lung (P for trend = 0.002) cancer. We found no association with phylloquinone intake. CONCLUSION: These findings suggest that dietary intake of menaquinones, which is highly determined by the consumption of cheese, is associated with a reduced risk of incident and fatal cancer.
http://www.ncbi.nlm.nih.gov/pubmed/20335553
High fat improve lipid profile:
http://www.ajcn.org/cgi/reprint/67/3/573S.pdf
As for you "healthy" cereal:
1. Heart attacks are caused/associated with small, dense subclass of low density lipoprotein (LDL).
The association of low-density lipoprotein (LDL) subclass patterns with coronary heart disease was investigated in a case-control study of nonfatal myocardial infarction. Subclasses of LDL were analyzed by gradient gel electrophoresis of plasma samples from 109 cases and 121 controls. The LDL subclass pattern characterized by a preponderance of small, dense LDL particles was significantly associated with a threefold increased risk of myocardial infarction, independent of age, sex, and relative weight
http://jama.ama-assn.org/cgi/content/abstract/260/13/1917
2. Low fat, high carb diets increase small, dense LDL (which cause heart attacks, see above):
With high-fat diets, 87 subjects had predominantly large, buoyant LDL (pattern A), whereas the remainder had primarily smaller, denser LDL (pattern B).
http://www.ajcn.org/cgi/content/abs...fbf6b2a821cbddf9972e7ddd&keytype2=tf_ipsecsha
3. Grains inhibit mineral absorbtion due to phytic acid:
The marked inhibitory effect of bran on iron absorption can almost completely be explained by its content of phytates. There are other inhibiting factor(s) as well in bran but they play only a minor role especially in meat containing meals. Several studies were made to clarify the role of phytates. Enzymatic dephytinization of bran almost fully removed its inhibiting effect. The same was observed when washing bran with hydrochloric acid. A "physiological" mixture of monoferric, potassium and magnesium phytates showed the same inhibition of the absorption of iron as bran with the same phytate content. There was a strong semilogarithmic relationship (r = 0.99) between the inhibition of iron absorption and the amount of phytates. As little as 5-10 mg phytate phosphorus added to a wheat roll containing 3 mg iron inhibited iron absorption by 50 per cent. Ascorbic acid as well as meat strongly counteracted this inhibition. It was concluded that if bran is used to increase the dietary fiber intake that would interfere with the absorption of iron. However, if the intake of ascorbic acid and/or meat are sufficiently increased in the bran containing meals that would effectively counteract the inhibition of the iron absorption by the phytates in bran (wheat fiber).
http://www.ncbi.nlm.nih.gov/pubmed/2820048
http://www.ncbi.nlm.nih.gov/pubmed/474478
Whole grain actually has more phytic acid than white:
BACKGROUND: Phytic acid has been reported to impair the absorption of minerals and trace elements such as calcium, zinc, and iron in humans. However, limited information is available on the effect of phytic acid on magnesium absorption. OBJECTIVE: The objective was to evaluate the effect of phytic acid on fractional apparent magnesium absorption in humans. DESIGN: Two stable-isotope studies were performed with 8-9 healthy adults per study. Test meals were based on 200 g phytic acid-free wheat bread; test meals with and without added phytic acid were served on days 1 and 3 according to a crossover design. Phytic acid was added in amounts similar to those naturally present in whole-meal (1.49 mmol) and in brown bread (0.75 mmol). Each test meal was labeled with 0.7 mmol (25)Mg or 1.1 mmol (26)Mg. The total magnesium content was standardized to 3.6 mmol in all test meals. Apparent magnesium absorption was based on fecal monitoring. RESULTS: The addition of phytic acid lowered fractional apparent magnesium absorption from 32.5 +/- 6.9% (no added phytic acid) to 13.0 +/- 6.9% (1.49 mmol added phytic acid; P < 0.0005) and from 32.2 +/- 12.0% (no added phytic acid) to 24.0 +/- 12.9% (0.75 mmol added phytic acid; P < 0.01). The inhibiting effect of phytic acid was dose dependent (P < 0.005). CONCLUSION: The results show that fractional magnesium absorption from white-wheat bread is significantly impaired by the addition of phytic acid, in a dose-dependent manner, at amounts similar to those naturally present in whole-meal and brown bread.
http://www.ncbi.nlm.nih.gov/pubmed/14985216
3.5. Minerals are important, because low magnesium & calcium are correlated with obesity in kids. They hypothesize that it's due to the effect of magnesium & calcium independently increasing insulin sensitivity:
http://aje.oxfordjournals.org/cgi/content/full/164/5/449
http://www.thecrimson.com/article/2004/1/21/magnesium-rich-foods-reduce-diabetes-risk-study/
4. More studies showing improvement of lipid profile:
CONCLUSIONS: Mediterranean and low-carbohydrate diets may be effective alternatives to low-fat diets. The more favorable effects on lipids (with the low-carbohydrate diet) and on glycemic control (with the Mediterranean diet) suggest that personal preferences and metabolic considerations might inform individualized tailoring of dietary interventions. (ClinicalTrials.gov number, NCT00160108.) 2008 Massachusetts Medical Society
http://www.ncbi.nlm.nih.gov/pubmed/18635428
There were significant decreases in fasting serum TAG (33%), postprandial lipemia
after a fat-rich meal (29%), and fasting serum insulin concentrations (34%) after men consumed the ketogenic
diet. Fasting serum total and LDL cholesterol and oxidized LDL were unaffected and HDL cholesterol tended to
increase with the ketogenic diet (11.5%; P 0.066). In subjects with a predominance of small LDL particles
pattern B, there were significant increases in mean and peak LDL particle diameter and the percentage of LDL-1
after the ketogenic diet. There were no significant changes in blood lipids in the control group. To our knowledge
this is the first study to document the effects of a ketogenic diet on fasting and postprandial CVD biomarkers
independent of weight loss. The results suggest that a short-term ketogenic diet does not have a deleterious effect
on CVD risk profile and may improve the lipid disorders characteristic of atherogenic dyslipidemia. J
http://jn.nutrition.org/cgi/reprint/132/7/1879
Also:
1. Fructose (from your sugar/sucrose rich cereal) causes hypertension:
http://www.nature.com/ki/journal/v74/n4/abs/ki2008184a.html
2. Fructose (from your sugar/sucrose rich cereal) causing leptin resistance (persistent hunger regardless of caloric intake). The rats basically ate themselves to death:
http://www.ncbi.nlm.nih.gov/pubmed/18703413
3. If any correlation can be drawn from the rise of obesity and changes in dietary habits from 1970-today, it's an increase of vegetable oils, decrease of animal fat, and increase of sugar/wheat:
http://wholehealthsource.blogspot.com/2008/12/us-weight-lifestyle-and-diet-trends.html
4. High protein, low carb diet improves body composition regardless of caloric intake:
http://www.ajcn.org/cgi/content/abstract/83/2/260
5. Lectins from grains causing leptin resistance:
http://www.biomedcentral.com/1472-6823/5/10