So I thought everyone just started their babies on cereal as the first solid food..then fruits and veggies down the road. At least it seems most people I know always mention cereal first. My doctor sent me some information on this when I asked him "so you mean I should start with fruits and veggies, NOT cereal?" His response:
Absolutely!!! You definitely want to start on fruits and veggies. You don't ever need cereals and would be better off if you never used them. Cereals are easy and kids love to eat them because they taste good and are crunchy, but they are directly converted to sugar in the blood stream and are the leading cause of type 1 diabetes. Cereals have no nutrition unless they have been fortified and those vitamins and minerals are not absorbed. You always want to use God made foods and not man made processed foods like cheerios and gold fish. This is the reason I sent this article out. The food industry has been taken over by fun, sugary and catchy named terrible food. Read the following and then we need to chat next time you are in.
Dr. B
JAMA. 2003 Oct 1;290(13):1713-20. (Journal of the American Medical Association)
Related Articles, Links
Comment in:
J Pediatr. 2004 May;144(5):684-5.
JAMA. 2003 Oct 1;290(13):1771-2.
Timing of initial cereal exposure in infancy and risk of islet autoimmunity.
Norris JM, Barriga K, Klingensmith G, Hoffman M, Eisenbarth GS, Erlich HA, Rewers M.
Department of Preventive Medicine and Biometrics, University of Colorado Health Sciences Center, Denver 80262, USA.
jill.norris@uchsc.edu
CONTEXT: Dietary exposures in infancy have been implicated, albeit inconsistently, in the etiology of type 1 diabetes mellitus (DM). OBJECTIVE: To examine the association between cereal exposures in the infant diet and appearance of islet autoimmunity (IA). DESIGN: Birth cohort study conducted from 1994 to 2002 with a mean follow-up of 4 years. SETTING: Newborn screening for HLA was done at St Joseph's Hospital in Denver, Colo. First-degree relatives of type 1 DM individuals were recruited from the Denver metropolitan area. PARTICIPANTS: We enrolled 1183 children at increased type 1 DM risk, defined as either HLA genotype or having a first-degree relative with type 1 DM, at birth and followed them prospectively. We obtained exposure and outcome measures for 76% of enrolled children. Participants had variable lengths of follow-up (9 months to 9 years). MAIN OUTCOME MEASURES: Blood draws for the detection of insulin autoantibody, glutamic acid decarboxylase autoantibody, or IA-2 autoantibody were performed at 9, 15, and 24 months and annually thereafter. Children with IA (n = 34) were defined as those testing positive for at least 1 of the autoantibodies on 2 or more consecutive visits and who tested positive or had diabetes on their most recent visit. RESULTS: Children initially exposed to cereals between ages 0 and 3 months (hazard ratio [HR], 4.32; 95% confidence interval [CI], 2.0-9.35) and those who were exposed at 7 months or older (HR, 5.36; 95% CI, 2.08-13.8) had increased hazard of IA compared with those who were exposed during the fourth through sixth month, after adjustment for HLA genotype, family history of type 1 DM, ethnicity, and maternal age. In children who were positive for the HLA-DRB1*03/04,DQB8 genotype, adjusted HRs were 5.55 (95% CI, 1.92-16.03) and 12.53 (95% CI, 3.19-49.23) for initial cereal exposure between ages 0 to 3 months and at 7 months or older, respectively. CONCLUSION: There may be a window of exposure to cereals in infancy outside which initial exposure increases IA risk in susceptible children.
Low Grain and Carbohydrate Diets Treat Hypoglycemia, Heart Disease, Diabetes Cancer and Nearly ALL Chronic Illness
by Joseph Brasco, MD
Unfortunately, the debate over the validity of this concept has primarily been waged in the media and lay publications and not in the scientific journals. Many of the popular books which support this position are gimmicky, and often, lack adequate scientific referencing. Yet, at their core is very important concept -- limiting the intake of carbohydrates, (especially as cereal grains and starches), will improve human health.
Some critics claim that reduced carbohydrate diets are a fashion trend. Well, this so called trend actually dates back some time. Anthropological study of early hominids has concluded that they lived as hunters-gathers. While nuts, seeds, vegetation and fruit made up an important part of the hunter- gather's diet, his mainstay was hunted or scavenged animal prey.
More recent evaluations of early man's nutritional patterns by Dr. Loren Cordain, estimate that as much as 65 percent of his calories were derived from animal products. Granted, early man was not eating corn fed Angus beef from Jewel, but he was eating the meat, the organs and the bones of his prey. Essentially, a high protein/fat diet. It was a mere 10,000 years ago (or less) that man began exploiting an agricultural niche.
This transition was made due to decreasing population of large game prey and an increasing population of humans. While undeniable good has transcended this dietary shift, i.e., growth of the human population, establishment of permanent settlements, the inception of civilization itself - man's health may have suffered in the transition.
Generally, in most parts of the world, whenever cereal-based diets were first adopted as a staple food replacing the primarily animal-based diets of hunter-gatherers, there was a characteristic reduction in stature, a reduction in life span, an increase in infant mortality, an increased incidence of infectious disease, an increase in diseases of nutritional deficiencies (i.e., iron deficiency, pellagra), and an increase in the number of dental caries and enamel defects.
In a review of 51 references examining human populations from around the earth and from differing chronologies, as they transitioned from hunter-gathers to farmers, one investigator concluded that there was an overall decline in both the quality and quantity of life.
There is now substantial empirical and clinical evidence to indicate that many of these deleterious changes are directly related to the predominately cereal-based diets of these early farmers. Since 99.99% of our genes were formed before the development of agriculture, from a biological perspective, we are still hunter-gathers.
Thus, our diet should reflect the sensibilities of this nutritional niche: lean meats; fish; seafood; low glycemic vegetables and fruit, (modern agriculture has significantly increased the sugar and starch content of vegetables and fruits over their Paleolithic counterparts), nuts and seeds - the evolutionary diet.
Glycemic Index
The term glycemic index, (GI) (a qualitative indicator of carbohydrate's ability to raise blood glucose levels), has seen a lot of mileage among the many non-ketogenic low carbohydrate diets. Most of these diets attribute the rise in obesity to the over consumption of high glycemic carbohydrates, and the subsequent over production of insulin.
While this may be an oversimplification, there is growing evidence to support a relationship between GI and non-insulin dependent diabetes (NIDDM), and obesity. In a prospective study of 65,000 US women, researchers were able to demonstrate that the dietary GI was positively associated with the risk of NIDDM.
The authors concluded that diets with a high GI increase insulin demand and thus cause hyperinsulinemia among patients with NIDDM, as well as in normal subjects. If chronic, this hyperinsulinemia can increase the risk for, as well as exacerbate NIDDM.
The issue of carbohydrates and insulin has more recently been addressed in a review article by Grundy. Grundy states that because secretion by pancreatic beta-cells is glucose sensitive, a high intake of carbohydrates has been reported to produce higher post prandial insulin levels. Moreover, it is possible that repeated stimulation of a high insulin output by high-carbohydrate diets could hasten an age-related decline in insulin secretion and lead to an earlier onset of NIDDM.
However, chronic hyperinsulinemia is not only associated with NIDDM, but is also related to a host of other medical conditions jointly known as Syndrome X. The constellation of disorders comprising Syndrome X include hypertriglyceridemia, increased LDL cholesterol, decreased HDL cholesterol, hypertension, hyperuricemia and obesity.
If high GI carbohydrates in fact contribute to chronic hyperinsulinemia as multiple studies suggest, they are likely to be causative of these other conditions as well. In addition to their role in hyperinsulinemia, studies have also linked high GI foods with overeating.
One study found an inverse relationship between satiety and both glycemic and insulin index. In another study,it was found that voluntary energy intake after a high GI meal was 53% greater than after a medium GI meal and was 81% greater than after the low GI meal. The authors concluded that a high GI meal promotes excessive food intake in obese subjects. The literature clearly points to a role of high GI carbohydrates in the development of insulin resistance and its subsequent disorders.
However, GI is obviously not the whole story. One researcher examined the insulin demand generated by isoenergetic portions of common foods. While some of the results were predictable, i.e., the fact that glucose and insulin sources were highly correlated, some were unexpected, i.e., some protein-based foods induced as much insulin secretion as did some carbohydrate rich foods. At first glance, these results seem confounding. However, if one looks at the broader function of insulin, they are consistent.
Insulin is not just responsible for glucose disposal, but for storage and uptake of multiple nutrients. Whether these other nutrients can result in a chronic hyperinsulinemic state, as seen with high GI diets, is not known; it is unlikely due to their compensatory effect on glucagon. The other major difference between the insulin response of other nutrients versus carbohydrate is their effect on blood glucose.
While protein and fat stimulate insulin response, their effect on glucose is minimal. This lack of effect on blood sugar is more than trivial difference. It actually may be the glycosylation of end organs (especially the pancreatic beta-cells) that ultimately leads to NIDDM and its associated conditions. Thus, while a hyperinsulinemic state is not desirable for human health under any circumstance, the combination of hyperinsulinemia with impaired glucose homeostasis is likely to prove even more deliterious.
While the current literature would support limiting the consumption of high GI foods, GI certainly does not provide the final answer. If one was to follow this concept literally (as some popular books suggest) one could argue that potato chips at a GI of 50-59% were more beneficial than carrots at a GIU of 90-99%.
A better way of looking at carbohydrates is to return to the principles of the "evolutionary diet." Robert Crayhon, M.S., author and champion of the "Paleolithic diet", divides carbohydrates into two basic groups, paleocarbs and neocarbs. Paleocarbs include vegetables, fruits and perhaps tubers. Neocarbs (carbohydrates introduced within the last 10,000 years or less), include grains, legumes, and especially flour products, which did not exist for most of human history.
The worst of the neocarbs include sugar and white flour products. If we follow the simple guidelines of restricting ourselves to paleocarbs, we will in general be eating fiber rich, nutrient dense, low glycemic carbohydrates, the best nature has to offer.
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Why you SHOULDN'T start on cereal first...
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