What Is Diabetes

Our bodies make sugar as a fuel for our cell’s energy furnaces. It releases it at constant low levels. Releasing too much at once is like flooding the engine in your car with too much gas. It makes it stall out.

For most of human history, we have had a high-fiber diet. This resulted in the carbohydrates and sugars in our diet being released very slowly and steadily into the bloodstream over many hours. Now we have almost 140 pounds of sugar per person per year being added into our diet in food processing. This represents 18 percent of our calories, causing massive spikes in blood sugar. This forces our bodies to prevent sugar from entering the cells too quickly. This change is called “insulin resistance.”

Insulin is the key that opens our cell furnaces so the sugar can get in to be burned for energy. When your cells become deaf to the insulin, the sugar builds up in your bloodstream instead. Meanwhile, the sugar can’t get into the cell to be burned for fuel and your cells are starving.

This is what occurs with insulin resistance. Meanwhile, your cells send out the message that they are energy starved, causing the body to make more sugar and more insulin. These high insulin levels, then proceed to turn the sugar into fat, causing you to pack on the pounds and become even more insulin resistant (thus the abdominal spare tire). The cycle continues until your body can no longer compensate and your blood sugar goes up. At that point you have developed diabetes, and your doctor will usually offer you whatever the newest, most profitable, and sadly often toxic medication the drug companies are marketing to them.

Why The Diabetes Epidemic?
Several factors are creating a perfect storm for diabetes developing. These include:

1. Excess sugar and white flour in the diet combined with low fiber.
2. Vitamin D deficiency, especially from the misguided advice to avoid sunshine. Sunshine makes vitamin D in our body. Low vitamin D is associated with not only diabetes, but also markedly increased risk for autoimmune illness, pain, hypertension, and other problems.
3. The obesity epidemic.
4. Decreased exercise.
5. Numerous chemicals in our environment, which block testosterone in men and increase testosterone in women.

Inadequate testosterone levels in men (imho anything under 500 ng/dl– research shows the “normal range” is to be an absurdity) have been shown to cause metabolic syndrome. This is a combination of high blood pressure, high cholesterol, and either diabetes or prediabetes. When you see a ‘spare tire’ developing on a gentleman’s abdomen, this is often the culprit. In women, the elevated testosterone is often associated with polycystic ovarian syndrome (PCOS), acne, facial hair growth, and even infertility. Metabolic syndrome improves with the treatments discussed below as well.

Testing
To screen for prediabetes, I will check a fasting insulin level. Ignore the normal range. If the fasting insulin is over 10 uIU/ ml, you should take measures now for prevention. Also check a glycosylated hemoglobin (HgBA1C). If it is over 5.8 percent, you may be developing prediabetes.

Diabetes Is Optional

In fact, this is the title of my newest book, now available on Amazon. It discusses the treatments below in-depth. Begin with simple things that help optimize blood sugar levels in your body. These include:

An Ounce Of Prevention—helping your body maintain healthy blood sugar regulation is:

1. Take a good multivitamin high in magnesium and vitamin D. My favorites are the Energy Revitalization System vitamin powder, or Clinical Essentials.
2. Cut back sugar intake. This doesn’t mean you can’t indulge your sweet tooth. In fact, chocolate in moderation is a health food. Begin by cutting out sodas and fruit juices, both of which have 3/4 teaspoon of sugar per ounce. This translates to 36 spoons of sugar in that 48 ounce “Big Burp” soda. Enjoy the whole fruit instead. Meanwhile, look at the nutritional label, and divide grams of sugar by four to see how many teaspoons of sugar are in a serving.
3. Go for walks in the sunshine. Or find other exercise, preferably outside, that you love.
4. Lose weight. This will be easier once you do the rest of the program and your insulin sensitivity improves. Research has shown that with adequate weight loss, diabetes actually goes away in 86 percent of diabetics.
5. Optimize testosterone levels in men. I will use bioidentical testosterone to bring the total testosterone up to about 900 ng/dl. In women, I would use the treatments discussed, along with the medications metformin and Aldactone to lower elevated testosterone.

Treating Diabetes

For childhood diabetes, which is a totally different autoimmune illness, insulin is a lifesaving and necessary treatment. For adult diabetics, it is a loan shark, which initially lowers blood sugar.

But because it often causes massive weight gain, it can worsen the diabetes in the long-term. So it may be necessary short-term, but it is not a good overall solution.

In my 40 years as a physician, I have found that most diabetes medications turn out to cause more harm and deaths than benefit. But routinely, physicians are not taught about the research on the drug’s toxicity until after the patent runs out and it is no longer profitable. Then the drug companies are off teaching them about the newest, most money-making, diabetes medication.

I don’t fault the drug companies for this. They are actually very nice people doing their job. Which is to make money. It is the physician’s job to be able to distinguish between what is real and truthful as opposed to slick advertising masquerading as science. But sadly, though exhorted to do so even by the past editors of the New England Journal of Medicine, they don’t realize the difference.

There is one medication that is an exception. It is an excellent medication called metformin, which is low cost and has withstood the test of time. It is highly effective, and well-tolerated. Its main toxicity is that it will sometimes cause nausea or diarrhea (lower the dose) and will routinely cause vitamin B12 deficiency unless someone is taking a multivitamin.

Hintonia Latiflora To The Rescue

From the high mountains of Central and South America, there is an amazing herb that can help lower blood sugars. This miracle botanical is an extract of the bark of a shrubby tree that grows in the Sonoran Desert. It’s been studied in detail for its ability to reverse high blood sugars for over 60 years. It has only recently become available to the North American public in a product called Sucontral-D.

There have been over a dozen studies showing how powerfully effective hintonia is!

How Does Hintonia Latiflora (Sucontral D) Work?
First, it is a rich source of a special family of flavonoids, called Coutareagenin. This polyphenol nutrient found in bark extracts unique to hintonia and appears to be responsible for many of its blood-sugar controlling benefits.

Mexican researchers also found that plant is an inhibitor of the enzyme alpha-glucosidase, which then slows the breakdown of carbohydrates in the food, mimicking the effect of a high-fiber diet.

What Does The Hintonia Research Show?
Solid research in numerous studies shows that not only can hintonia help control blood sugar and overcome insulin resistance, reducing your need for pharmaceuticals. It can also enhance the effectiveness of diabetes medications if your doctor and you decide that you need them.

For example, in a study published in the German journal Naturheilpraxis mit Naturalmedizin (Naturopathic Practice with Natural Medicine), Hintonia latiflora significantly lowered HgBA1C values (average levels of blood sugar), fasting glucose levels (blood sugar before a meal) and postprandial (after eating) blood sugar levels.

Fasting and after meal blood glucose numbers, along with A1C levels, are important because they show how much sugar circulates through your system and how your body deals with it after meals. What the research showed was amazing! Fasting and post-meal blood sugars improved by an impressive 23 and 24 percent respectively with hintonia. And glycosylated hemoglobin decreased by a remarkable average of 0.8 points (about 11 percent)! This means many people went from being diabetic to no longer being diabetic.

Impressively, by the end of the study 39 percent of those using anti-diabetes drugs could reduce their medication levels. Some were able to stop their medication entirely.

But there is more good news. Hintonia not only lowered blood sugar and often reversed diabetes. It also eliminates many of the symptoms of diabetes an impressive 73 percent over time. This is a massive change that can dramatically increase your quality of life, and well-being.

Participants also saw improvements in blood pressure, lipids, and liver values.

People with diabetes struggle with blood sugars that spike and plummet during the day and night. As this occurs, your energy, pain and mental clarity may find themselves on a roller coaster as well. One of hintonia’s greatest benefits is that it helps keep those sugars steady throughout the day and night, making life easier and contributing to long-term better glucose control.

The president of the International Diabetes Foundation was the lead author on another study that strongly recommended the use of this unique herb in treating and preventing Type 2 diabetes. Not only because of improved blood sugar control, but also because of its effectiveness in lowering cholesterol and other elements of metabolic syndrome that can lead to Type 2 diabetes.

So the bottom line? Diabetes is optional!

The post Diabetes Is Optional appeared first on Total Health Magazine.

• Kidneys can be diseased by 90 percent before tests ever indicate a problem.
• Liver disease is often detected after the liver is 70 percent diseased.
• Heart disease has often been developing 20 years before traditional tests reveal a problem.
• Breast cancer is usually detected with a mammogram, which is eight to ten years before cancer begins to develop.
• Diabetes tests include the AIC test, which often detects a problem five to ten years after it could have been detected.
• Alzheimer’s cannot be detected, by conventional medicine, until there is a beginning of loss in cognitive function.
• Parkinson’s Disease is only detected when a slight trembling occurs in one finger of one hand. By then about 80 percent of all dopamine receptors in the brain have died or been seriously damaged.

Disease usually happens in five distinct stages:

1. Stressed cells happen when there is poor nutrition,high toxin levels, high stress levels and genetic or biochemical deficiencies.
2. Weakened cells occur when cells have been stressed too long, and cells lose their energy level.
3. Dysfunctional cells are the third stage of deterioration when cells begin to experienced functional challenges. This is when most traditional tests detect a problem, such as high blood pressure, high glucose or chest pain known as angina.
4. Mutated cells occur when the nucleus of the cell becomes damaged and can no longer produce a healthy replacement cell.
5. Diseased cells happen when the cell cannot function and begins to damage other neighboring cells.

The post The Early Detection of Chronic Disease appeared first on Total Health Magazine.

The Types Of Diabetic Neuropathies

According to the National Institutes of Health², DNs are most common in those who have problems controlling their blood glucose levels, those with high blood lipid levels (i.e., cholesterol and triglycerides), those with high blood pressure and those who are overweight.

Other factors can also contribute to the cause. The risk increases with age and with the length of time a person has diabetes. Those who have had diabetes for at least 25 years have the highest rates of neuropathy.

There are different types of DNs, with their own symptoms:³

• Peripheral neuropathy is the most common type of DN. It causes pain or loss of feeling in the toes, feet, legs, hands, and arms.
• Changes in digestion, bowel and bladder function, sexual response, and perspiration take place in autonomic neuropathy; the nerves that serve the heart and control blood pressure, as well as nerves in the lungs and eyes, may be affected as well. Hypoglycemia unawareness, a condition in which people no longer experience the warning symptoms of low blood glucose levels, may also occur.
• Proximal neuropathy results in thigh, hip, or buttocks pain, and leads to weakness in the legs.
• Sudden weakness of one nerve or a group of nerves, causing muscle weakness or pain, is caused by focal neuropathy. In this case, any nerve in the body can be affected.

DIETARY SUPPLEMENTS

There are a number of dietary supplements with the potential to help in the treatment of DN. Some of the most promising are acetyl-L-carnitine, alpha lipoic acid, benfotiamin, gamma-linolenic acid and methylcobalamin.

Acetyl-L-Carnitine
Acetyl-L-carnitine (ALC) is a form of the amino acid L-carnitine. Both have similar roles in helping to transport fat into muscle cells where it can be burned for energy. Also, the “acetyl” part of ALC helps produce the acetylcholine, a brain chemical, which is required for various mental functions. ALC occurs naturally in the brain, liver and kidneys.

ALC has been shown to be deficient in diabetics.⁴ In double-blind research, type 1 or type 2 diabetics with peripheral neuropathy experienced improved symptoms after taking 1500–3000 mg ALC daily in divided doses for a year. ALC seems to increase nerve fibers, regenerate clusters of nerve fibers, and improve sensations. In patients who have pain as the most significant symptoms, taking ALC 1000 mg two to three times daily also decreases neuropathy-related pain within six months of beginning treatment. Lower doses (500 mg three times daily) do not seem to reduce pain. ALC also seems more likely to be effective for reducing pain in patients with a shorter duration of diabetes and patients with poorly-controlled type 2 diabetes.^5,6,7,8 In research, the best response was associated with using 1,000 mg ALC, three times daily.

Orally, acetyl-L-carnitine is generally well tolerated. One gram daily of L-carnitine seems to significantly increase the anticoagulant effects of acenocoumarol.^9,10 Acenocoumarol is an oral anticoagulant similar to warfarin, but shorter-acting. This interaction has only been reported with L-carnitine, but theoretically could occur with acetyl-L-carnitine.

Alpha Lipoic Acid
Alpha lipoic acid (ALA) is a natural antioxidant manufactured by the body and similar to certain vitamins. Unlike most other antioxidants, however, it has the advantage of being soluble in both fat and water, so it can provide production both inside and outside of cells.¹¹ ALA is also found in some foods, particularly liver and yeast.

Giving 600 mg to 1200 mg oral or intravenous ALA daily reduced symptoms of peripheral neuropathy in diabetics. ALA improved symptoms such as burning, pain, numbness, and prickling of the feet and legs. It also seems to improve objective measures such as ratings of nerve function decline and disability. Symptom improvement occurs within three to five weeks with oral and intravenous dosing.^{12,13,14,15,16,17,18,19,20} Doses lower than 600 mg daily have not been shown to be effective.²¹ Furthermore, other research shows that ALA can also contribute to reducing blood sugar levels and insulin sensitivity.^22,23,24,25 A daily dosage range of 600 mg to 1200 mg ALA is likely to yield positive results.

Skin rash has been reported in some individuals after using oral doses of alpha-lipoic acid.²⁶ Theoretically, use with other hypoglycemic drugs might cause additive blood sugar lowering effects.²⁷

Benfotiamin
Benfotiamin is a particularly well-absorbed form of vitamin B1. Double-blind research in diabetics demonstrated that oral doses of 400 mg daily resulted in a statistically significant improvement in neuropathy score in the treatment group compared to placebo. The most significant improvement reported was pain decrease in polyneuropathy (a type of peripheral neuropathy).²⁸ Other research has demonstrated statistically significant effectiveness in reducing diabetic neuropathy pain with daily doses ranging between 150–320 mg benfotiamin.²⁹ In addition, studies have also shown that benfotiamin in combination with other B vitamins is effective in the treatment of DNs.³⁰ Best results will probably be seen with 400 mg of benfotiamin daily.

Benfotiamin has a good tolerance profile without any adverse effects, and no established drug interactions.

Gamma Linolenic Acid
Gamma linolenic acid (GLA) is an omega-6 fatty acid commonly found in evening primrose oil (derived from the seeds of the evening primrose plant) as well as black currant seed oil and borage oil. The body converts GLA into an anti-inflammatory, hormone-like substance called prostaglandin E1. In addition to DN, GLA has shown benefit in the treatment of eczema³¹, fibrocystic breast disease³², premenstrual syndrome³³ and rheumatoid arthritis.³⁴

In double-blind research, taking oral doses of 360 to 480 mg GLA daily for six months to one year reduced symptoms and prevents nerve deterioration in peripheral neuropathy patients who have type 1 or type 2 diabetes.^35,36,37,38 It seems to be more effective in patients with better glucose control compared to patients with poor glucose control.³⁹ Take 360 to 480 mg GLA daily. It may take six months or longer for results.

Orally, gamma-linolenic acid (GLA) can cause mild gastrointestinal effects such as nausea, vomiting, soft stools, diarrhea, flatulence, and belching.^40,41,42 GLA might prolong bleeding time.⁴³ GLA appears to have anticoagulant effects.⁴⁴ Theoretically, taking GLA with other anticoagulant or anti-platelet drugs might increase the risk of bruising and bleeding.

Methylcobalamin
Methylcobalamin is a well-absorbed form of vitamin B12. In double-blind research, daily oral supplementation of 1500 mcg methylcobalamin by diabetics resulted in significant improvements in autonomic neuropathy compared to placebo.⁴⁵ Other research also demonstrated similar benefits and improvements in autonomic neuropathy when methylcobalamin was given orally or as an injection.^46,47

Orally and intramuscularly, vitamin B12 does not usually cause adverse effects, even in large doses. Limited case reports suggest that chloramphenicol (an antimicrobial drug) can delay or interrupt the response of immature red blood cells to supplemental vitamin B12 in some patients.⁴⁸ A daily dose of 1500 mcg methylcobalamin is appropriate.

Conclusion
Just in case you’re wondering, you can use any or all of these dietary supplements indicated at the same time. Other than the adverse reactions listed, there are none associated with the concurrent use of more than one supplement.

References:

2. Diabetic Neuropathies: The Nerve Damage of Diabetes. NIH Publication No. 08–3185. Bethesda, MD: National Diabetes Information Clearinghouse, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health. February 2008. Retrieved October 3, 2008 from http://diabetes.niddk.nih.gov/dm/pubs/neuropathies/
3. Ibid. Diabetic Neuropathies.
4. Ibid. Diabetic Neuropathies.
5. Sima AAF, Calvani M, Mehra M, et al. Acetyl-L-carnitine improves pain, nerve regeneration, and vibratory perception in patients with chronic diabetic neuropathy: An analysis of two randomized, placebo-controlled trials. Diabetes Care 2005;28:89–94.
6. Onofrj M, Fulgente T, Melchionda D, et al. L-acetylcarnitine as a new therapeutic approach for peripheral neuropathies with pain. Int J Clin Pharmacol Res 1995;15:9–15.
7. De Grandis D, Minardi C. Acetyl-L-carnitine (levacecarnine) in the treatment of diabetic neuropathy. A long-term, randomised, double-blind, placebo-controlled study. Drugs R D 2002;3:223-31.
8. Quatraro A, Roca P, Donzella C, et al. Acetyl-L-carnitine for symptomatic diabetic neuropathy. Diabetologia 1995;38:123.
9. Sima op. cit.
10. Martinez E, Domingo P, Roca-Cusachs A. Potentiation of acenocoumarol action by L-carnitine. J Intern Med 1993;233:94.
11. Bachmann HU, Hoffmann A. Interaction of food supplement L-carnitine with oral anticoagulant acenocoumarol. Swiss Med Wkly 2004;134:385.
12. Kagan V, Khan S, Swanson C, et al. Antioxidant action of thioctic acid and dihydrolipoic acid. Free Radic Biol Med 1990;9S:15.
13. Ziegler D, Hanefeld M, Ruhnau K, et al. Treatment of symptomatic diabetic polyneuropathy with the antioxidant alpha-lipoic acid: A 7-month, multicenter, randomized, controlled trial (ALADIN III Study). Diabetes Care1999;22:1296–301.
14. Reljanovic M, Reichel G, Rett K, et al. Treatment of diabetic polyneuropathy with the antioxidant thioctic acid (alphalipoic acid): A 2-year, multicenter, randomized, double-blind, placebo-controlled trial (ALADIN II). Alpha Lipoic Acid in Diabetic Neuropathy. Free Radic Res 1999;31:171–7.
15. Ziegler D, Hanefeld M, Ruhnau KJ, et al. Treatment of symptomatic diabetic peripheral neuropathy with the antioxidant alpha-lipoic acid: A 3-week, multicenter, randomized, controlled trial (ALADIN Study). Diabetologia 1995;38:1425–33. 15.
16. Ruhnau KJ, Meissner HP, Finn JR, et al. Effects of 3-week oral treatment with the antioxidant thioctic acid (alpha-lipoic acid) in symptomatic diabetic polyneuropathy. Diabet Med 1999;16:1040–3.
17. Ametov AS, Barinov A, Dyck PJ, et al. The sensory symptoms of diabetic polyneuropathy are improved with alpha-lipoic acid. Diabetes Care2003;26:770-6.
18. Ziegler D, Nowak H, Kemplert P, et al. Treatment of symptomatic diabetic polyneuropathy with the antioxidant alpha-lipoic acid: A meta-analysis. Diabet Med 2004;21:114–21.
19. Negrisanu G, Rosu M, Bolte B, Lefter D, Dabelea D. Effects of 3-month treatment with the antioxidant alpha-lipoic acid in diabetic peripheral neuropathy. Rom J Intern Med 1999;37:297–306.
20. Zeigler D, Schatz H, Conrad F, Gries FA, Ulrich H, Reichel G. Effects of treatment with the antioxidant alpha-lipoic acid on cardiac autonomic neuropathy in NIDDM patients. A 4-month randomized controlled multicenter trial (DEKAN Study). Deutsche Kardiale Autonome Neuropathie. Diabetes Care 1997;20:369–373.
21. Tankova T, Cherninkova S, Koev D. Treatment for diabetic mononeuropathy with alpha-lipoic acid. Int J Clin Pract 2005;59:645–650.
22. Sachse G, Willms B. Efficacy of thioctic acid in the therapy of peripheral diabetic neuropathy. Hormone Metab Res Suppl 1980;9:105–7.
23. Konrad T, Vicini P, Kusterer K, et al. Alpha-lipoic acid treatment decreases serum lactate and pyruvate concentrations and improves glucose effectiveness in lean and obese patients with Type 2 diabetes. Diabetes Care 1999;22:280–7.
24. Jacob S, Henriksen EJ, Tritschler HJ, et al. Improvement of insulin-stimulated glucose-disposal in type 2 diabetes after repeated parenteral administration of thioctic acid. Exp Clin Endocrinol Diabet 1996;104:284–8.
25. Jacob S, Henriksen EJ, Schiemann AL, et al. Enhancement of glucose disposal in patients with type 2 diabetes by alphalipoic cid.Arzneimittelforschung 1995;45:872–4.
26. Jacob S, Ruus P, Hermann R, et al. Oral administration of RAC-alpha-lipoic acid modulates insulin sensitivity in patients with type-2 diabetes mellitus: a placebo-controlled, pilot trial.Free Rad Biol Med 1999;27:309–14.
27. Vincent HK, Bourguignon CM, Vincent KR, Taylor AG. Effects of alpha-lipoic acid supplementation in peripheral arterial disease: a pilot study. J Alt Complement Med 2007;13:577–84.
28. Konrad, op. cit.
29. Haupt E, Ledermann H, Kopcke W. Benfotiamine in the treatment of diabetic polyneuropathy—a three-week randomized, controlled pilot study (BEDIP study). Int J Clin Pharmacol Ther 2005;43:71–77.
30. Winkler G, Pál B, Nagybéganyi E, Ory I, Porochnavec M, Kempler P. Effectiveness of different benfotiamine dosage regimens in the treatment of painful diabetic neuropathy. Arzneimittelforschung 1999;49(3):220–4.
31. Head KA. Peripheral neuropathy: pathogenic mechanisms and alternative therapies. Altern Med Rev 2006; 11(4):294–329.
32. Schalin-Karrila M, Mattila L, Jansen CT, et al. Evening primrose oil in the treatment of atopic eczema: effect on clinical status, plasma phospholipid fatty acids and circulating blood prostaglandins. Br J Dermatol 1987;117:11–9.
33. Mansel RE, Pye JK, Hughes LE. Effects of essential fatty acids on cyclical mastalgia and noncyclical breast disorders. In Omega-6 Essential Fatty Acids: Pathophysiology and Roles in Clinical Medicine, ed. DF Horrobin. New York: Alan R Liss, 1990, 557–66.
34. Puolakka J, Makarainen L, Viinikka L, Ylikorkola O. Biochemical and clinical effects of treating the premenstrual syndrome with prostaglandin synthesis precursors. J Reprod Med 1985;30:149–53.
35. Pullman-Mooar S, Laposata M, Lem D, et al. Alteration of the cellular fatty acid profile and the production of eicosanoids in human monocytes by gamma-linolenic acid. Arthritis Rheum 1990;33:1526–33.
36. Jamal GA. The use of gamma linolenic acid in the prevention and treatment of diabetic neuropathy. Diabet Med 1994;11:145–9.
37. Horrobin DF. The use of gamma-linolenic acid in diabetic neuropathy. Agents Actions Suppl 1992;37:120–44.
38. Jamal GA, Carmichael H. The effect of gamma-linolenic acid on human diabetic peripheral neuropathy: a double-blind placebo-controlled trial. Diabet Med 1990;7:319–23.
39. Keen H, Payan J, Allawi J, et al. Treatment of diabetic neuropathy with gamma-linolenic acid. The gamma-Linolenic Acid Multicenter Trial Group. Diabetes Care 1993;16:8–15.
40. Ibid.
41. Leventhal LJ, Boyce EG, Zurier RB. Treatment of rheumatoid arthritis with gammalinolenic acid. Ann Intern Med 1993;119:867-73.
42. Zurier RB, Rossetti RG, Jacobson EW, et al. Gamma-linolenic acid treatment of rheumatoid arthritis. A randomized, placebo-controlled trial. Arthritis Rheum 1996;39:1808-17.
43. Keen op. cit.
44. Guivernau M, Meza N, Barja P, Roman O. Clinical and experimental study on the long-term effect of dietary gamma-linolenic acid on plasma lipids, platelet aggregation, thromboxane formation, and prostacyclin production. Prostaglandins Leukot Essent Fatty Acids 1994;51:311–6.
45. Ibid.
46. Yaqub BA, Siddique A, Sulimani R. Effects of methylcobalamin on diabetic neuropathy. Clin Neurol Neurosurg 1992; 94:105–111.
47. Yoshioka K, Tanaka K. Effect of methylcobalamin on diabetic autonomic neuropathy as assessed by power spectral analysis of heart rate variations. Horm Metab Res 1995; 27:4–44.
48. Ide H, Fujiya S, Asanuma Y, et al. Clinical usefulness of intrathecal injection of methylcobalamin in patients with diabetic neuropathy. Clin Ther 1987; 9:183–192.
49. Tatro DS, ed. Drug Interactions Facts. Facts and Comparisons Inc., St. Louis, MO. 1999.

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The good news is your “diabetes” may even be reversible when your statin treatment is over. I’ve counted 84 people (including my BookFace mom) who got off their statin and reversed their “diabetes.”

It may be news to you, but many studies and reports have shown that statins can cause raise blood sugar, which is sadly and disgracefully mistaken for “diabetes.” Now you’re on the expensive medication merry-go-round!

Another bombshell coming: People with high cholesterol have a lower risk of getting diabetes, which is in keeping with what I just told you about statins triggering the condition. I’ve got the most current information now. Researchers looked at the rates of diabetes among 63,385 Dutch residents in the Netherlands between 1994 and 2014. Of these participants, 25,137 had inherited “Familial Hypercholesterolemia” which is a condition that means high cholesterol from their inherited genes. These people with the genetic snp (pronounced snip) coding for high cholesterol displayed significantly lower rates of type 2 diabetes! The details were reported in the March 2015 edition of JAMA if you want to look it up. The prevalence of type 2 diabetes was actually 38% lower, which suggests high cholesterol protects against diabetes. Keep in the back of your mind how people taking statin drugs face an increased risk of developing diabetes, anywhere from 9 to 46 percent depending on what study you read.

It’s pure genius if you think about it. Here you have multiple studies showing how cholesterol-reducing statins raise blood sugar, and now we see clearly that people who have higher endogenous levels of cholesterol are protected from diabetes. I’m talking about endogenous (body-produced) cholesterol, okay, so this is not your excuse to eat bacon.

Insulin is your God-given pancreatic hormone and it’s secreted to help reduce blood sugar after you eat and drink. You want some insulin to maintain blood glucose levels, but too much of it is the equivalent of acid in your veins. And guess what? The use of statin drugs appears to increase your insulin levels!

Now I’ll summarize this:

• High insulin and blood sugar is extremely harmful to your health.
• The regulation of glucose and insulin is crucial.
• The ‘standard of practice’ in medicine calls for severely low levels of cholesterol (in my opinion) hence the need for statins.
• Statins reduce cholesterol, but may raise insulin and blood sugar over time.
• Medications used to reduce blood sugar do not address the full-body inflammatory process that is going on.
• If you started a statin drug, and now have diabetes, try to lower your cholesterol with diet and exercise, and don’t lower it too much.

The post The Diabetes Statin Connection appeared first on Total Health Magazine.