Discover the Truth about Lower Back Pain Causes

When most people think of lower back pain causes, they immediately think of injuries caused by lifting items improperly or sitting at a desk for an extended period of time. Those things certainly cause the majority of the lower back pain that doctors treat every day. However, they aren't the only causes of lower back pain.

One of the lower back pain causes that is often overlooked is a kidney infection. Obviously, not all lower back pain will be caused by a kidney infection but it should definitely be kept in mind, especially if a person doesn't recall injuring their back in any way, shape, or form recently. Kidney infections are often accompanied by a fever. Most often, the fever can spike rather high. Kidney infections are a serious emergency and need to be treated right away. If left untreated, permanent kidney damage can result.

Another potential lower back pain cause is having a spine that isn't aligned properly. Proper alignment of the spine is crucial not for just lower back health but body health in general. Pinched nerves and reduced blood flow can result if a person's spine is even the tiniest bit out of alignment. Thankfully, a misaligned spine is easy to fix.

A trip to the chiropractor's is usually all that's needed to get everything straight again. If the problem is particularly bad or been left untreated for a long time, multiple trips might be needed to get everything perfectly in alignment again. Fortunately, most chiropractor appointments are inexpensive. Even if you don't have insurance or your insurance doesn't cover a chiropractor, you should still be able to afford the appointments you'll need.

A pinched nerve is also one of the lower back pain causes. Pinched nerves can be extremely painful, depending on where the nerve is pinched at. You can get a shooting pain from a pinched nerve when you move certain ways. Occasionally, the pain can even feel like a constant stabbing pain. Either way, a pinched nerve will need to be diagnosed and treated by a doctor.

Obviously, the most common lower back pain causes are muscle injuries of one sort or another. Muscle injuries tend to be throbbing in nature while nerve injuries feel like stabbing, shooting pains. Since muscle injuries to the lower back are fairly common, it's easy to find products you can purchase over the counter to help ease the aches and pains you may be feeling. Medications, heat wraps, and ice are commonly prescribed. Exercise and stretching can help heal an injured lower back quickly and prevent injuries from happening in the future.

Lower back pain doesn't need to be a part of life. It can be avoided all together in most instances. All you need to do is listen to what your body is telling you, learn proper lifting techniques, and become familiar with the various lower back pain causes. Being educated about them will help prevent injuries in the future.

Tips About The Causes Of Lower Back Pain

There can be a wide variety of causes for lower back pain. For instance, repetitive injuries at work, improper lifting techniques, and poor posture are but a few of the more common ones. There are also other things that can be causes of lower back pain such as various illnesses and diseases.

Kidney infections are one of the prime causes of lower back pain that often go undiagnosed, ultimately resulting in disastrous consequences. An undiagnosed kidney infection can cause severe damage to a person’s kidneys. Once a kidney is scarred or otherwise damaged, it’s impossible to heal. If too much damage is done, it can cause a kidney to stop functioning entirely. If a kidney stops functioning, a person will be on dialysis for the rest of their life or will need a kidney transplant. Anytime you have lower back pain that’s accompanied by a fever, you must see a doctor immediately in order to rule out a kidney infection as the culprit.

Pinched nerves are also one of the causes of lower back pain. When discussing nerves, it’s important to note that nerve pain and muscle pain feel different. Nerve pain is typically a sharp, stabbing, or shooting pain. Muscle pains are more aching, throbbing, or tearing pains. Knowing the differences in the two kinds of pains should help you determine exactly what is causing the pain to begin with. If it’s a pinched nerve, you will need to seek treatment at a doctor’s office. Various tests can be done to determine which nerve is pinched and what is causing it to become pinched. From there, a treatment plan can be discussed. A pinched nerve can become permanently damaged so it’s important to get treatment for it right away to prevent that from happening.

Perhaps the most obvious causes of lower back pain are muscle related injuries. They can happen in a wide variety of ways. Muscle strains and sprains are perhaps the most common. Active sports, using improper techniques when lifting or exercising, pretty much anything you do that requires use of a muscle in the your back can cause lower back injuries and pain. It’s important to be aware at all times of what you’re doing and how you’re doing it if you wish to avoid injuring your back. If you have any questions about a particular exercise or lifting technique or need any help whatsoever with lifting an item or exercising, don’t hesitate to ask. It just may mean the difference between a healthy back and a serious injury.

While there are certainly many different causes of lower back pain, they can be easily treated with the proper mix of rest, exercise, and occasionally medication. If at all possible, it’s best to avoid an injury to your lower back entirely to begin with, however that’s not always possible. At the very least, now that you know more about the causes of lower back pain, you know how to handle it better.

Type 1 Diabetes Mellitus and Possible Causes of It

Type 1 diabetes, or Insulin Dependent Diabetes Mellitus (IDDM), is a disease characterized by "auto-destruction" of the pancreatic beta cells that produce insulin. Overtime, your body silently destroys these cells creating an insulin deficiency. IDDM appears to stem from an inherited defect in the immune system, triggered by some environmental stimuli. The exact cause of the disease is still unknown; however, scientists have isolated a few factors that may be related to development of the disease. The purpose of this review is to provide insight on where research is headed and what we already know about the progression of IDDM.

Genetics

Recent mapping of the human genome has opened many areas to explore in the field of diabetes research. Animal models and large population studies have led to some possible genetic links. The major histocompatibility complex (MHC) on chromosome 6 is a regulator of immune response because it recognizes "self" and "not-self" things in the body. If something is seen as foreign, the MHC will stimulate antibody production. Genes encoded on the MHC are associated with IDDM, particularly the human leukocyte antigen (HLA) class II alleles, DQ and DR (1). Although the HLA-DQ locus appears to be the best single marker for susceptibility among Caucasians, at least 40% of family-related diabetes cases have combinations of both DQ and DR alleles (2,3). DQ and DR alleles are almost always found together on a chromosome and the risk is associated with them not being in equilibrium. Many combinations have been documented, some showing both increased and decreased susceptibility, however it has been difficult to determine the contribution of HLA-DQ independent of DR. The insulin gene region at chromosome 11 is also associated with IDDM risk.

Studies conducted in the 1970's established an HLA association and contribution of IDDM while comparing siblings with the disease (4,5,6). When comparing the relationship between family members, results are inconsistent. Current estimates suggest that HLA is 40-50% related to genes passed down by family members (7,5). The risk of developing IDDM for a twin of someone who already has the disease is about 70%, and this rises depending on the specific HLA alleles that the twins share (8). When comparing the risk of developing the disease for first-degree relatives vs. the US population, the risk is 1/20 and 1/300, respectively (1). Research in the area of HLA has been extremely difficult. Definitive answers cannot be drawn because not everyone holding these "susceptible" genes develops IDDM. Actually, less than 10% of genetically susceptible individuals progress to diabetes, implying that other factors are responsible for progression of the disease. Researchers have explored these other factors, particularly environmental factors such as early introduction of cow's milk, dysregulation of the gut immune system, viral infections, drinking water and a number of others.

Cow's Milk

Several population studies have found a link between exposure to cow's milk and increased risk for IDDM in genetically susceptible individuals. A few studies have also shown an increased risk for infants exposed to cow's milk or cow's milk based formulas within the first 3 months, and also later in life. It has been found that infants fed cow's milk had increased levels of bovine insulin anti-bodies compared to those that were breast-fed (9,10,11). Bovine insulin is found in the milk of cows. The antibodies binding to bovine insulin appear to cross-react with human insulin (9,10). Bovine insulin is considered immunogenic because it differs from human insulin by 3 amino acids.

Insulin-specific antibodies (ISA), those specific for IDDM, and increased T cell levels from exposure to cow's milk have been found in those carrying diabetes associated HLA risk alleles. Of all the studies to date however, levels of insulin binding antibodies seem to decrease as the child approaches 9-18 months. This suggests that the infant is building a tolerance to dietary antigens (12). However, Vaarala et al. discovered that infants who developed ISA's, also had increased levels of bovine insulin antibodies, suggesting that insulin specific immune responses in children prone to develop autoimmunity cannot be prevented (12). Other studies have found bovine insulin antibody levels to decrease when human insulin was presented in the body.

Early weaning (2-3 months) from breast milk has been shown to increase the risk for IDDM. Maternal milk contains colostrum, a light fluid that contains a variety of protective factors for the infant. Infants have an immature and easily penetrable gut system allowing food, in this case cow's milk, to easily cross into the bloodstream. The gut system works in one of two ways: it will either accept (build tolerance to) or reject (develop immunity to) food and its dietary components (13). Several cow's milk proteins have been shown to be related to IDDM such as bovine albumin, beta-lactoglobulin, and beta casein (14,15,16)

A study by Karjalainen et al. in 1992 was conducted to assess whether bovine serum albumin (BSA) was a trigger for IDDM (14). Researchers measured the levels of anti-BSA and anti-ABBOS (specific part of the albumin protein) antibodies in the serum of children with newly diagnosed IDDM, children without IDDM, and blood donors' (14). Antibodies that react to the ABBOS also react with a beta cell surface protein that may represent a target for autoimmune attack (14). All children in the study with IDDM had the highest amount of both antibodies, especially ABBOS, compared to the children without IDDM and blood donors' (14). Antibody levels declined after one or two years of exposure to cow's milk (14). This suggests that albumin has a section that is capable of reacting with "beta-cell specific surface proteins", which could contribute to islet cell dysfunction because of molecular mimicry (14). What is molecular mimicry?

When an antigen is present in the body, T cells latch onto a short segment, consisting of about 10 amino acids. T cells then present the antigen to macrophages that engulf it and break it down into smaller protein fragments. The macrophages bring the fragments to the cell surface where capable T cells can bind to it. This activates the T cells, leading to stimulation in other areas to attack all proteins with similar amino acid segments. Bovine serum albumin has a short amino acid sequence similar to a beta cell surface receptor ICA69 (17) and beta casein shares a similar sequence with a glucose transporter. If molecular mimicry occurs here, then presentation of BSA or beta casein in the body would lead to autoimmune destruction.

Contrary to Karjalainen et al.'s study, Vaarala et al. found no association with BSA, but did find an increased risk for newly diagnosed IDDM with beta-lactoglobulin, another cow's milk protein (15). A study conducted by Cavallo et al. found an association with increased risk of newly diagnosed IDDM with beta casein, another milk protein (16). However, no differences were noted with BSA and other proteins assessed (16). Despite these conflicting results, it does appear that some form of "cross-reactivity" may occur with cow's milk proteins and islet-cell antigens, leading to "auto-attack" of the beta cells.

The role of cow's milk related to IDDM is not clear. The hypothesis of molecular mimicry has been questioned. Few studies have found a link between cellular immunity to BSA and IDDM. A recent study found that reactivities to beta casein were similar between newly diagnosed individuals with IDDM, their immediate relatives without the disease, and non-related healthy subjects. One confounding factor of the previous study was the lack of appropriately matched subjects, because researchers failed to use HLA matched relatives. Also, when comparing breast-feeding vs. cow milk formula, it is unclear at what point there is an increased risk, as well as the actual amount needed to induce an immune response. Despite all of the evidence presented here, exposure to cow's milk and risk for IDDM is only suggestive because the exact cause is unknown (18).

Viral Infections

Viral infections have been considered to be "more" responsible for diabetes development, than milk proteins. Identifying the exact virus responsible has been extremely daunting for several reasons. Individuals are exposed to many viral infections within their lifetime. Although IDDM is primarily a juvenile disease, by the time the disease is diagnosed, children have been exposed to many viruses. Thus, pinpointing the exact one would be every difficult, if not impossible to link. Another problem is that immunological damage often occurs after the virus is gone, leaving no trace of the virus responsible. However, large population studies, as well as human and mice studies, have led to some possible viruses responsible.

Coxsackie B Virus

Coxsackie B virus is an enterovirus, a virus part of a group of picornaviruses, related to those that cause polio. Several studies have found that after or with exposure to Coxsackie B that individuals developed IDDM. Also, large population studies have found antibodies against the virus in children with newly diagnosed IDDM. Coxsackie B viruses have been isolated from the pancreas in children who have developed IDDM very rapidly. Plus, inducing certain mouse strains with the virus has caused these mice to develop the disease.

Molecular mimicry has been postulated in the case of Coxsackie B virus. The virus increases the expression of an enzyme GAD in the pancreas. GAD is a highly potent autoantigen of the autoimmune response in humans and mice models. Coxsackie B and GAD share a similar sequence that may lead to cross reactivity.

Other, but not limited to, factors that may be responsible for Coxsackie B and IDDM are altered immune system regulation because of viral infection, altered memory of the T cells causing them to forget which are "self" and "not self" in the presence of viral infection, and persistent infection of the beta cells because of viral antigens expressed within them.

Although this all sounds promising, several other studies have not found conflicting results such as no difference in Coxsackie B antibodies between those with IDDM and those without it, along with no differences in prevalence and amount of antibodies responsible.

Rubella Virus

About 12-20% of fetal infected individuals with rubella will develop diabetes within 5-20 years (19,20). In some adults, development of diabetes has occurred after infection with rubella. Although this poses a threat to genetically susceptible individuals, vaccination programs have decreased the amount of rubella cases.

Cytomegalovirus (CMV)

There have been individual case reports of children developing IDDM after exposure to CMV. There have been recent studies done showing that newly diagnosed individuals with IDDM were recently exposed to CMV. It has been suggested that molecular mimicry may be partly responsible because CMV proteins share a resemblance with a protein in the islet cells of the pancreas. Pak et al. discovered that about 20% of individuals with IDDM have CMV DNA in the islet cells (21). Despite all this evidence however, a large Swedish study found no correlation between CMV infection and risk for IDDM (22). Besides all of this, vaccinations against the virus have lowered the prevalence of CMV infections.

Epstein-Barr Virus (EBV)

Individual cases have been noted where those infected with EBV develop diabetes. However, IDDM development as a result of EBV infection is probably not responsible for the disease in the majority of subjects. Little research and single cases are not enough to consider this a major cause.

Other Viruses

There have been reports of individuals developing IDDM after exposure to influenza, hepatitis A, varicella zoster, mumps, measles, rotavirus, polio, and Coxsackie A virus.

Other Environmental Factors

Recent studies have found a positive association between zinc levels in drinking water and protection against diabetes. Magnesium levels in tap water have been shown to be related to diabetes protection as well, however conflicting evidence resides with this. The protections that zinc may provide is unclear. Despite possible relationships with heavy metals and diabetes, more research must be done to ascertain the actual relationship.

Of all the evidence presented here, researchers have been unable to find the exact cause for development of IDDM. What we do know is that genetically susceptible individuals have an increased risk for diabetes. As displayed here, researchers have located genes that seem to predispose individuals to diabetes. Genes are not enough however, because not everyone who has these genes develops diabetes. Environmental factors are another part of the picture. Whether it is milk proteins, viral infections, or impaired gut function, those with genetic susceptibility tend to develop the disease after exposure to these. Identifying which factor is responsible has been difficult because exact mechanisms of the body are still unclear and tests to determine these things may not be specific or have not yet been developed. Plus, isolating one factor is not reasonable because there are a lot of overlaps in immune functions and genetics. All in all, research is headed in the right direction, but for now there is still no known cause for IDDM.

References

1. Gottlieb MD, P.A., Eisenbarth MD, Ph.D., G.S. Diagnosis and Treatment of Pre-Insulin Dependent Diabetes. Annual Review of Medicine. 1998; 49: 397-405.

2. Nepom G.T. Immunogenics and IDDM. Diabetes Review. 1993; 1: 93-103.

3. Pugliese A, Eisenbarth G.S. Human Type 1 Diabetes Mellitus: Genetic Susceptibility and Resistance. In Type 1 Diabetes: Molecular, Cellular, and Clinical Immunology, ed. G.S. Eisenbarth, K.J. Lafferty. New York: Oxford University Press. 1996; pp.

4. 134-152.

5. Singal DP, Blajchman MA. Histocompatibility (HL-A) Antigens, Lymphocytotoxic Antibodies and Tissue Antibodies in Patients with Diabetes Mellitus. Diabetes. 1973; 22: 429-432

6. Thomsen M, Platz P, Andersen OO et al. MLC Typing in Juvenile Diabetes Mellitus and Idiopathic Addisons Disease. Transplant Review. 1975; 22: 125-147

7. Nerup J, Platz P, Andersen OO et al. HLA Antigens and Diabetes Mellitus. Lancet. 1974; ii: 864-866.

8. Risch N. Assessing the Role of HLA-Linked and Unlinked Determinants of Disease. American Journal of Human Genetics. 1987; 40: 1-14.

9. Verge C.F., Gianani R, Yu L, et al. Late Progression to Diabetes and Evidence for Chronic Beta Cell Autoimmunity in Identical Twins of Patients with Type 1 Diabetes. Diabetes. 1995; 44:1176-1179.

10. Vaarala O, et al. Cow Milk Feeding Induces Antibodies to Insulin in Children-A Link Between Cow Milk and Insulin-Dependent Diabetes Mellitus? Scandinavian Journal of Immunology. 1998; 47: 131-135.

11. Vaarala O, et al. Cow Milk Feeding Induces Primary Immunization to Insulin in Infants at Genetic Risk for Type 1 Diabetes. Diabetes. 1999; 48: 1389-1394.

12. Paronen J, et al. The Effect of Cow Milk Exposure and Maternal Type 1 Diabetes on Cellular and Humoral Immunization to Dietary Insulin in Infants at Genetic Risk for Type 1 Diabetes. Diabetes. 2000; 49: 1657-1665.

13. Vaarala O, et al. Cow's Milk Formula Feeding Induces Primary Immunization to Insulin in Infants at Genetic Risk for Type 1 Diabetes. Diabetes. 2000; 49(10):1657-1665.

14. Strobel S, Mowat A. Immune Responses to Dietary Antigens: Oral Tolerance. Immunology Today. 1998; 19: 173-181.

15. Karjalainen J, et al. A bovine albumin peptide as a possible trigger of insulin-dependent diabetes mellitus. New England Journal of Medicine. 1992; 327(5):302-307.

16. Vaarala O, et al. Cellular Immune Response to Cow's Milk B-lactoglobulin in Patients with Newly Diagnosed IDDM. Diabetes. 1996; 45: 178-182.

17. Cavallo M.G., et al. Cell-Mediated Immune Response to B Casein in Recent-Onset Insulin-Dependent Diabetes: Implications for Disease Pathogenesis. Lancet. 1996; 348: 926-928.

18. Virtanen S.M., et al. Cow's Milk Consumption, HLA-DQB1 Genotype, and Type 1 Diabetes Mellitus. A Nested Case-Control Study of Siblings of Children with Diabetes. Diabetes. 2000; 49: 912-917.

19. Vaarala O. The Gut Immune System and Type 1 Diabetes. Annals of the New York Academy of Sciences. 2002; 958: 39-46.

20. Menser M.A., et al. Rubella Infection and Diabetes Mellitus. Lancet. 1978; 1: 57-60.

21. McIntosh E.D., et al. A Fifty-Year Follow Up of Congenital Rubella. Lancet. 1992; 340: 414-415.

22. Pak C.Y., et al. Association of Cytomegalovirus Infection with Autoimmune Type 1 Diabetes. Lancet. 1988; 2: 1-4.

23. Ivarsson S.A., et al. The Prevalence of Type 1 Diabetes Mellitus at Follow-Up of Swedish Infants Congenitally Infected with Cytomegalovirus. Diabetes Medicine. 1993; 10: 521-523.

Chris Theberge is the founder of the Nutrition and Food Web Archive, NutriWeb Designs, and Dietitian Designs. Visit http://www.nafwa.org for free nutrition and food-related resources.

Diabetes - Causes and Prevention

Diabetes mellitus (sometimes called "sugar diabetes") is a condition that occurs when the body can't use glucose (a type of sugar) normally. Glucose is the main source of energy for the body's cells. The levels of glucose in the blood are controlled by a hormone called insulin, which is made by the pancreas. Insulin helps glucose enter the cells.

In diabetes, the pancreas does not make enough insulin (type 1 diabetes) or the body can't respond normally to the insulin that is made (type 2 diabetes). This causes glucose levels in the blood to rise, leading to symptoms such as increased urination, extreme thirst, and unexplained weight loss.

Types of Diabetes

Type 1 diabetes (previously known as insulin-dependent diabetes)

Type 1 diabetes is an auto-immune disease where the body's immune system destroys the insulin-producing beta cells in the pancreas. This type of diabetes, also known as juvenile-onset diabetes, accounts for 10-15% of all people with the disease. It can appear at any age, although commonly under 40, and is triggered by environmental factors such as viruses, diet or chemicals in people genetically predisposed. People with type 1 diabetes must inject themselves with insulin several times a day and follow a careful diet and exercise plan.

Type 2 diabetes (previously known as non-insulin dependent diabetes)

Type 2 diabetes is the most common form of diabetes, affecting 85-90% of all people with the disease. This type of diabetes, also known as late-onset diabetes, is characterised by insulin resistance and relative insulin deficiency. The disease is strongly genetic in origin but lifestyle factors such as excess weight, inactivity, high blood pressure and poor diet are major risk factors for its development. Symptoms may not show for many years and, by the time they appear, significant problems may have developed. People with type 2 diabetes are twice as likely to suffer cardiovascular disease. Type 2 diabetes may be treated by dietary changes, exercise and/or tablets. Insulin injections may later be required.

Gestational diabetes mellitus (GDM)

GDM, or carbohydrate intolerance, is first diagnosed during pregnancy through an oral glucose tolerance test. Between 5.5 and 8.8% of pregnant women develop GDM in Australia. Risk factors for GDM include a family history of diabetes, increasing maternal age, obesity and being a member of a community or ethnic group with a high risk of developing type 2 diabetes. While the carbohydrate intolerance usually returns to normal after the birth, the mother has a significant risk of developing permanent diabetes while the baby is more likely to develop obesity and impaired glucose tolerance and/or diabetes later in life. Self-care and dietary changes are essential in treatment.

Causes Of Diabetes

Diabetes can be caused by too little insulin (a hormone produced by the pancreas to control blood sugar), resistance to insulin, or both.

To understand diabetes, it is important to first understand the normal process of food metabolism. Several things happen when food is digested:

A sugar called glucose enters the bloodstream. Glucose is a source of fuel for the body.

An organ called the pancreas makes insulin. The role of insulin is to move glucose from the bloodstream into muscle, fat, and liver cells, where it can be used as fuel.

People with diabetes have high blood sugar. This is because their pancreas does not make enough insulin or their muscle, fat, and liver cells do not respond to insulin normally, or both.

There are three major types of diabetes:

Type 1 diabetes is usually diagnosed in childhood. The body makes little or no insulin, and daily injections of insulin are needed to sustain life.

Type 2 diabetes is far more common than type 1 and makes up most of all cases of diabetes. It usually occurs in adulthood. The pancreas does not make enough insulin to keep blood glucose levels normal, often because the body does not respond well to the insulin. Many people with type 2 diabetes do not know they have it, although it is a serious condition. Type 2 diabetes is becoming more common due to the growing number of older Americans, increasing obesity, and failure to exercise.

Gestational diabetes is high blood glucose that develops at any time during pregnancy in a woman who does not have diabetes.

Diabetes affects more than 20 million Americans. About 54 million Americans have prediabetes. There are many risk factors for diabetes, including:

1. A parent, brother, or sister with diabetes

2. Obesity

3. Age greater than 45 years

3. Some ethnic groups (particularly African Americans, Native Americans, Asians, Pacific Islanders, and Hispanic Americans)

4. Gestational diabetes or delivering a baby weighing more than 9 pounds

5. High blood pressure

6. High blood levels of triglycerides (a type of fat molecule)

7. High blood cholesterol level

8. Not getting enough exercise

The American Diabetes Association recommends that all adults over age 45 be screened for diabetes at least every 3 years. A person at high risk should be screened more often.

How To Prevent Or Control Diabetes

Diabetes prevention is proven, possible, and powerful. Studies show that people at high risk for type 2 diabetes can prevent or delay the onset of the disease by losing 5 to 7 percent of their body weight. You can do it by eating healthier and getting 30 minutes of physical activity 5 days a week. In other words: you don't have to knock yourself out to prevent diabetes. The key is: small steps that lead to big rewards. Learn more about your risk for developing type 2 diabetes and the small steps you can take to delay or prevent the disease and live a long, healthy life.

Small Steps. Big Rewards. Your GAME PLAN to Prevent

Watch Your Diet

There is no one magic diet that works for everyone. Nor is there a single diet that works best for one individual over a long time. Pay attention to your genetics, and to your ethnic group's traditional foods. If you are African American, that does not mean overcooked vegetables or pork rinds. Such garbage came on the nutritional scene only recently, and is not a true ethnic food. The same is true for Italians who overdose on pepperoni pizza. Being Italian myself as, well as having enjoyed fantastic African cuisine, I can tell you there is a lot more to these diets than the recent introductions often associated with these cultural groups.

Except for Eskimos and a few other highly specialized ethnic groups, all diets must adhere to the same few macronutrient rules. For example:

Eliminate as many processed carbohydrates as possible.

Don't eat carbohydrates 2 hours before bedtime.

Balance your fat/carbos/protein in a roughly 30-40-30 ratio (this is a guideline, not a hard and fast rule--it doesn't work for everyone).

Eat at least 5 or 6 small meals a day.

Always eat a high-protein breakfast.

Did you know that the peanuts offered on airlines are LESS fattening than the fat-free pretzels?
It's true. Stay away from fat-free foods--they make your insulin levels do a yo-yo, and that makes you put on fat. Yuck. Worse, it sets the stage for adult-onset diabetes.

Do NOT eat white flour, bleached flour, enriched flour, or any other kind of wheat flour that is not whole wheat. The glycemic effects of such flours will work against you. Eat whole grain flours, and try to get a variety. Amaranth and soy are two good flours. Eat oat groats instead of oatmeal. In short, get your grains in the least-processed form you can. This holds true for everyone, regardless of genetics (unless you have a malabsorption problem). This one "trick" will help you keep your insulin level on an even keel, and that is paramount to diabetes prevention and management.

What also holds true for everyone is: drink lots of water! Fill a gallon jug twice a day, and make sure you drink all of it. Once you get as lean as you want to be, cut back to a single gallon if you want to. For added fat loss, drink chilled (but not super cold) water. Sodas do not count. Such beverages are extremely unhealthy, for reasons I won't cover here. However, I will say that if you want to get osteoporosis, soft drinks are for you. Soft drinks make for soft bones.

Make sure to eat at least 5 or 6 small meals a day, rather than one big one. Doing so levels out your insulin and your blood sugar. Forget about that full feeling. If you find yourself overeating out of anxiety or boredom, fix the underlying problem -- don't add to it by poor eating!

Stay Healthy.

My Name is Abayomi Aje, I have written many articles concerning weight loss and other health related articles some of which can be found on my blog at http://yourhealthdoctor.blogspot.com