The reason for a healthy eating plan for those diagnosed with type 2 diabetes is to help to make your everyday dining easier and to also help to:

• reduce and stabilize your insulin and blood sugar levels
• gain or maintain a healthy body weight
• achieve normal cholesterol and triglyceride levels
• achieve a blood pressure reading lower than 140/80 mm/HG

The best healthy eating plan is one that includes food choices which adequately cover your known nutritional requirements for:

• vitamins
• minerals
• anti-oxidants
• essential amino acids
• essential fatty acids
• fiber
• protein
• low-glycemic index (low-GI) carbohydrates

Eating more plant foods and adequate animal protein will generally help your type 2 diabetes control.

Some carbohydrates aren’t even listed in the glycemic index because they don’t include enough carbs to affect your blood sugar levels. This list of foods includes:

• artichokes, asparagus,
• broccoli
• cabbage, raw carrots, cauliflower, celery, celery root, cucumber
• eggplant, endive
• fennel
• green beans
• kale
• lettuce
• mushrooms, mustard greens
• okra, onions
• parsley, pea pods, peppers
• radicchio, radishes
• sauerkraut, scallions, spinach, squash (summer)
• tomatoes
• turnip greens, turnips
• water chestnuts, watercress
• zucchini

Other foods also very low in carbohydrates (low-GI), with a “0″ glycemic index, include:

• avocados…even though they have a “0″ GI factor, they are considered a fat and a suitable serving size would be a quarter of a small avocado
• nuts and seeds… these too are fats and one tablespoon of seeds or six to ten nuts is recommended as a serving size

The proportion of carbohydrates, protein and fat varies in a healthy eating plan for a person with type 2 and depends on many factors. These include both physical and medical needs, therefore it is important to have an individual consultation with an Accredited Practising Dietitian who specializes in type 2 diabetes. The dietitian will also take into account all your needs, which will include your food likes and dislikes.

US researchers have discovered that leptin therapy can significantly improve the symptoms of patients with different forms of lipodystrophy.

Lipodystrophy is a rare condition that can be genetic or acquired and is characterized by loss of adipose tissue, low levels of leptin, dyslipidemia, severe insulin resistance, and diabetes.

In this study, Phillip Gordon and fellow researchers, from the National Institutes of Health in Bethesda, Maryland, carried out a prospective open-label study of leptin replacement therapy in 48 patients with acquired and inherited forms of lipodystrophy.

The median baseline age of the participants was 18 years, but ranged from 8 to 68 years, and 81% of the participants were female.

Recombinant methionyl human leptin was used to treat the patients at doses ranging from 0.04??”0.24 mg/kg/day. The participants were treated for varying periods of time, with 43 patients continuing therapy for at least 4 months, and 35 patients for at least 12 months.

Writing in the journal Diabetologia, the authors report that 12 months treatment with leptin lead to significant improvements in serum triglycerides, total cholesterol, and glycated hemoglobin (HbA1c) levels. There was also a nonsignificant trend for improvement in low-density lipoprotein cholesterol concentration, but high-density lipoprotein cholesterol levels were unaffected.

In patients who were treated for 12 months or more, triglyceride levels fell by 6.02 mmol/l (533.19 mg/dl), total cholesterol by 1.78 mmol/l (68.83 mg/dl), and HbA1c decreased by 1.5% from baseline.

Of note, proteinuria was also reduced with leptin replacement, the researchers report.

“Lipodystrophy is a complex condition with many different etiologies, but the primary metabolic derangement in this condition appears to be caused by leptin deficiency,” comment Gordon et al.

“We confirm that leptin administration is effective in ameliorating the major metabolic abnormalities seen in lipodystrophy,” they conclude.

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a part of Springer Science+Business Media. © Current Medicine Group Ltd; 2009

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A Belgian study has found that the natural sweetner stevioside reduces atherosclerosis in obese insulin-resistant mice.

Stevioside treatment was associated with increased adiponectin and insulin sensitivity and improved antioxidant defense in both the adipose tissue and the vascular wall, leading to inhibition of atherosclerotic plaque development and inducing plaque stabilization, the researchers report.

“Stevioside is a non-caloric natural sweetener that does not induce a glycemic response, making it attractive as sweetener to diabetics and others on carbohydrate-controlled diets,” note B Geeraert and team from the Catholic University of Leuven.

They looked at the effects of the sweetener on the expression of factors involved in the regulation of adipose tissue maturation, insulin signaling, inflammation and oxidative stress in the adipose tissue and aorta in relation to atherosclerosis in obese insulin-resistant mice.

In all, 14 mice were treated with 10 mg/kg stevioside and 20 with placebo for 12 weeks.

Stevioside treatment had no effect on weight and triglyceride levels, but lowered levels of glucose and insulin, improved adipose tissue maturation, and increased glucose transport, insulin signaling and antioxidant defense in white visceral adipose tissue, compared with placebo. These increases were in turn associated with a two-fold increase in adiponectin.

Stevioside also reduced plaque volume in the aortic arch by decreasing the macrophage, lipid and oxidized low-density lipoprotein content of the plaque, and increased expression of the antioxidant superoxide dismutases (Sods) 1,2 and 3. Circulating adiponectin was associated with improved insulin signaling and antioxidant defense in both the adipose tissue and the aorta of stevioside-treated mice.

Writing in the International Journal of Obesity, the researchers conclude: “The improved antioxidant defense can be attributed mainly to increased expressions of Sods.”

They recommend large-scale studies in humans and suggest that “the action of stevioside for preventing insulin resistance in obese persons requires further attention.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2009

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Combination therapy with fenofibrate and simvastatin does not provide additional protection against cardiovascular disease (CVD) in high-risk patients with Type 2 diabetes compared with simvastatin alone, according to findings from the ACCORD lipid trial.

Presenting the findings at the 59th Annual Scientific Session of the American College of Cardiology, in Atlanta, Georgia, USA, Henry Ginsberg (Columbia University College of Physicians and Surgeons, New York, USA) said that the findings “provide physicians with important new information regarding the treatment of a common lipid abnormality affecting many of their patients with Type 2 diabetes”.

The findings were also simultaneously published online in the New England Journal of Medicine.

For the ACCORD (Action to Control CardiOvascular Risk in Diabetes) lipid trial, 5518 people who had Type 2 diabetes and either pre-existing CVD or at least two additional CV risk factors and who were already taking simvastatin were randomly assigned to additional treatment with fenofibrate 54??”160 mg/day or placebo.

At baseline, the average total cholesterol level was 175 mg/dl (4.5 mmol/l), and the average high-density lipoprotein (HDL), low-density lipoprotein (LDL), and triglyceride levels were 101 mg/dl (2.6 mmol/l), 38 mg/dl (0.98 mmol/l), and 162 mg/dl (1.83 mol/l), respectively.

After a mean follow-up of 4.7 years, there was no significant difference between the two groups in the annual rate of the primary outcome (CV death, nonfatal heart attack, or nonfatal stroke) at 2.2% in patients taking fenofibrate and simvastatin and 2.4% in patients taking simvastatin and placebo. Annual rates of death were 1.5% in the fenofibrate group and 1.6% in the placebo group.

The researchers also compared rates of the primary outcome in 10 prespecified subgroups based on baseline characteristics. Of these, there appeared to be a difference between men and women taking combination therapy, “with the data for women suggesting potential harm and the data for men suggesting potential benefit,” Ginsberg reported. But the results did not reach statistical significance for either group.

There was also a trend toward benefit of fibrate treatment in a prespecified subgroup of patients with particularly high triglyceride levels of at least 204 mg/dl (2.30 mmol/l) and low HDL levels of 34 mg/dl (0.88 mmol/l). In these patients, the primary outcome rate was 12.4% in those taking fenofibrate plus simvastatin versus 17.3% in the simvastatin plus placebo arm. This compared with a rate of 10.1% in both study groups for all other participants.

“This dyslipidemia group outcome, which was prespecified, is concordant with several post hoc analyses from prior lipid trials,” Ginsberg noted.

He cited the Helsinki Heart Study (HHS) of gemfibrozil, which had a positive result for the primary outcome in the whole cohort and a greater benefit in a dyslipidemia subgroup, similar to that reported here. Other trials included the Bezafibrate Infarction Prevention (BIP) study and the Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study, which despite having negative results for the whole cohort showed significant findings for subgroups with severe dyslipidemia.

Ginsberg concluded: “ACCORD lipid does not support use of the combination of fenofibrate and simvastatin compared to simvastatin alone, to reduce CV events in the majority of patients with Type 2 diabetes mellitus who are at high risk for CVD.”

He added: “Subgroup analyses suggesting heterogeneity in response to combination therapy by gender or by the presence of significant dyslipidemia require further investigation.”

MedWire (www.medwire-news.md) is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2010

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The majority of people with diabetes do not understand the cause of type 2 diabetes. It is not your fault, it probably has not been explained to you. The root of the problem is insulin resistance and this can be found years before diabetes is even diagnosed.

People who have impaired glucose tolerance and even a large percentage with normal glucose tolerance, show their pancreas is producing plenty of insulin. Their cells are resisting its efforts and therefore glucose is not allowed to enter the cells. Maybe this means it would be beneficial to include a C-peptide test in your yearly health review as well as fasting blood sugar levels?

The result of a C-peptide test will show your health care provider if your blood sugar levels may be controlled by diet, weight loss and exercise or if you require insulin-stabilizing medications.

Research shows:

• there is a breakdown in signaling between your cells and this prevents insulin, which is a hormone, doing its job
• this hormone, a chemical messenger, is prevented from allowing glucose to enter your cells
• your cells simply know the glucose is there but it is not allowed to enter because of the missing link
• the pancreas produces more of this hormone and then both blood sugars and insulin-levels are raised
• in the early stages of insulin resistance the message is eventually heard. Glucose is then allowed to enter your cells and your blood sugars return to normal levels. This is known as compensated insulin-resistance.
• over time the stress of excessive insulin-production wears out the pancreas and it cannot keep up with the excessive production

When insulin-levels are consistently elevated, a long list of complications can follow. This is why type 2 diabetes is often associated with a number of other serious medical conditions:

• central or abdominal obesity
• high blood pressure
• abnormalities in cholesterol and triglyceride levels
• increased risk of heart disease and strokes
• polycystic ovary disease

The safest and most effective way to reduce insulin resistance in overweight and obese people, is through weight loss and increased physical activity. And you do not need to lose massive amounts to make a major contribution towards reducing the risk of a heart attack.

If you decide to have one health care provider for hypertension, and another for type diabetes, you could end up taking a multitude of drugs. The ideal is to find a health care provider who understands what is the cause of type 2 diabetes and treats you as a whole, working with you towards reducing your bloods sugar levels, lowering your insulin resistance, your cholesterol levels and your weight.