Vitamin E and α-lipoic acid prevent cardiovascular
and metabolic changes by comprising a …

Regenerative Antioxidant Protocol
To which are added new benefits from cinnamon and berberine
By Will Block

The sigh of History rises over ruins, not over landscapes, and in the Antilles there are few ruins to sigh over, apart from the ruins of sugar estates and abandoned forts.
— Derek Walcott, “The Antilles: Fragments of Epic Memory: the Nobel lecture”

S ugar consumption has risen dramatically in the U.S. over the last few decades. That’s not surprising when you consider that sugar is a significant component of pop beverages, along with most processed and prepared foods. In fact, it is hard to find a table without its ever presence, handy for sweetening your coffee or tea. Because sugar is unquestionably a root cause of overweight, obesity, metabolic disorder, insulin resistance, and type 2 diabetes—all of which are apt to drive succession to the next stage of degenerated health—this is grim news.

According to the Economic Research Service of the United States Department of Agriculture, per capita consumption of sugar and associated sweeteners grew by 19% between 1979 and 2003.1 Annual corn sweetener consumption was up by 400% during the same period. The consequence of this sugar rampage is most apparent when one considers data compiled by the Center for Disease Control and Prevention (CDC): childhood obesity now affects approximately 12.5 million children and teens (17% of that population).2 Furthermore, obesity prevalence has spiraled upwards from the 1960s, showing a rapid increase in the 1980s and 1990s, when it tripled among children and teens, from nearly 5% to approximately 15%. While it may have leveled off in the last 10 years, other deleterious changes continue, especially “among the heaviest boys, a significant increase in obesity has been observed, with the heaviest getting even heavier.” On top of that, substantial racial/ethnic disparities exist. Chiefly, Hispanic boys and non-Hispanic black girls are disproportionately affected by obesity. Furthermore, older children and teens are more likely to be obese compared with preschoolers.

While it used to be called
adult onset diabetes,
this is no longer true.

Adolescents Closing in on Adults

Obesity is the single greatest predictor of diabetes, and not surprisingly, as per the CDC, there has been a major shift to a lower age for the onset of type 2 diabetes.3 While it used to be called adult onset diabetes, this is no longer true. In children and adolescents, diabetes is one of the most common chronic diseases. Data indicate that about 151,000 people below the age of 20 years have diabetes. However, it is hard to detect type 2 diabetes in children because children may have no symptoms or mild symptoms, so estimates are probably on the short side. Also, it is difficult to be sure it is type 2 because criteria for differentiating between types of diabetes in children are confusing. That is, children with type 2 diabetes can develop ketoacidosis (acid build-up in the blood). Children with type 1 can be overweight. And because the overall prevalence of the disease is still quite low (a smaller percentage of the adolescent population has it), scientists have to sample a very large population of children in order to find a reasonable estimate of its prevalence.

New results suggest that
adequate antioxidant therapy can
both prevent and reverse the
metabolic and cardiovascular damage
in type 2 diabetes.

What Can Be Done?

You can’t forget the children, but adults are far more likely to suffer the consequences of type 2 diabetes. So it is with ourselves that our attention needs to be concentrated. As we have written before, and as you have undoubtedly heard numerous times, type 2 diabetes is a lifestyle disease. Meaning, it can almost assuredly be defeated by adopting a reasonable low-calorie, low-fat, and preferably low-glycemic diet, combined with an exercise and supplement program.

But in this economy, such a program is not always the easiest to achieve. In fact, for many worried about paying the mortgage and dealing with rising prices for fuel and food, changing lifestyle can be costly and time consuming. Not that it isn’t a worthwhile goal. However, aside from diabetic drugs, which all have untoward side effects, there is a lot that one can do to slow down the juggernaut of diabetes inevitability.

A fixed combination of α-lipoic acid
and vitamin E (either α-tocopherol or
tocotrienol-rich fraction) normalized
glucose tolerance, blood pressure,
and cardiac collagen deposition.

Vitamin E and α-Lipoic Acid Prevent and Reverse Sugar-Related Damage

In a new study, Australian researchers set out to determine whether the metabolic and cardiovascular changes induced in young adult male rats by a diet high in sugar could be prevented or reversed by chronic intervention with natural antioxidants.4 A regenerative antioxidant protocol, consisting of α-lipoic acid together with vitamin E (α-tocopherol alone or a tocotrienol-rich fraction) was administered in the food, to test the protocol for possible prevention or reversal of deleterious changes.

Without the antioxidant protocol, the rats developed glucose intolerance, hypertension, and increased collagen deposition in their hearts together with an increased ventricular stiffness. Ventricular stiffness makes it more difficult for blood to enter from the atrium. As a result, pressure rises in the atrium thereby increasing hydrostatic pressure of the pulmonary venous system and thus promoting pulmonary edema. However, a fixed combination of α-lipoic acid (1.6 g/kg food) and vitamin E (either α-tocopherol or tocotrienol-rich fraction, 0.84 g/kg food) normalized glucose tolerance, blood pressure, and cardiac collagen deposition. As well, the antioxidant protocol prevented and reversed ventricular stiffness in the sugar-fed rats. These results suggest that adequate antioxidant therapy can both prevent and reverse the metabolic and cardiovascular damage in type 2 diabetes.

Cinnamon Lowers Glycated Hemoglobin and Blood Pressure

In another recent study, English researchers investigated the blood glucose lowering effect of cinnamon on glycated hemoglobin (HbA1c), blood pressure, and lipid profiles in people with type 2 diabetes.5 Fifty-eight type 2 diabetic patients (25 males and 33 females), with a mean age of 54.9 years who were treated only with hypoglycemic agents and who had an HbA1c of more than 7% were randomly assigned to receive either 2 g of cinnamon or placebo daily for 12 weeks. Ingeniously, cinnamon was placed under the placebo bottle cap to foil identification.

Cinnamon should be considered
as an additional dietary supplement
option to regulate blood glucose and
blood pressure levels, even if one is
already taking conventional
medications to treat
type 2 diabetes mellitus.

After this intervention, the mean HbA1c was significantly decreased in the cinnamon group (8.22% to 7.86%) compared with placebo group (8.55% to 8.68%). At the same time, mean systolic and diastolic blood pressures (SBP and DBP) were also significantly reduced after 12 weeks in the cinnamon group (SBP: 132.6 to 129.2 mmHg and DBP: 85.2 to 80.2 mmHg) compared with the placebo group (SBP: 134.5 to 134.9 mmHg and DBP: 86.8 to 86.1 mmHg).

A significant reduction in fasting plasma glucose, waist circumference, and body mass index was observed at week 12 compared to baseline in the cinnamon group. However, the changes were not significant when compared to the placebo group. There were no significant differences in serum lipid profiles of total cholesterol, triglycerides, or HDL and LDL cholesterols; neither between nor within the groups. In the final conclusion, ingestion of 2 g of cinnamon per day (½ g with breakfast, 1 g with lunch, and ½ g with dinner) for 12 weeks significantly reduces the means of HbA1c, SBP, and DBP among poorly controlled type 2 diabetes patients. Therefore, cinnamon should be considered as an additional dietary supplement option to regulate blood glucose and blood pressure levels, even if one is already taking conventional medications to treat type 2 diabetes mellitus.

Mulberry Helps Control Blood Sugar

In a very recent study conducted at Ewha Women’s University in Seoul, Korea, researchers examined the ability of the active components in mulberry leaf extract (MLE) to inhibit intestinal glucose absorption.6 The researchers took note that carbohydrate digestion by the enzyme α-glucosidase and subsequent glucose uptake at the brush border (a dense layer of tiny protuberances that lines some absorbing cells in the intestine) are critical for postprandial blood glucose control. Consequently, any agent that can specifically inhibit this process can help prevent hyperglycemia by reducing blood sugar levels.

The single mulberry component 1-deoxynojirimycin (DNJ) has recently been viewed as the major mechanism of mulberry, dwarfing the activity of mulberry’s other blood sugar compounds. In this study, that was not true. In fact, the array of active components in MLE was found to provide higher potency in inhibiting intestinal glucose absorption compared to the single component DNJ. Thus MLE may be recognized as a promising inhibitor of intestinal glucose absorption.

For the inhibition of α-glucosidase, both MLE and DNJ were found effective. But in Caco-2 cells—a continuous line of heterogeneous human epithelial colorectal adenocarcinoma cells, developed by the Sloan-Kettering Institute for Cancer Research—only MLE showed significant inhibition of 2-deoxyglucose uptake. In these cells, DNJ was ineffective.

Furthermore, for glucose loading, administration of MLE produced potent inhibitions of glucose responses, far more so than DNJ in rats. This was not the case, however, for maltose (a malt sugar found in cereals such as barley) loading. Altogether, these findings were unexpected and demonstrate that the unabsorbed phytochemicals in MLE compete with glucose for intestinal glucose transporters. DNJ does not do this.

The array of active components in
mulberry leaf extract were
found to provide higher potency in
inhibiting intestinal glucose
absorption compared to
the single component

The scientists also evaluated the timing of MLE consumption, finding that if it is administered 30 min before glucose loading, the incremental area under the curve (IAUC) is significantly lower in rats, as compared to a simultaneously administered group. At the same time, cellular glucose uptake was significantly reduced in Caco-2 cells after pretreatment.

Berberine Improves Glucose Metabolism by Inhibition of Hepatic Gluconeogenesis

Originally identified in traditional Chinese herbal medicine, Chinese goldthread (Coptis chinensis) contains the compound berberine, now recognized as a powerful agent for health. In prior research, berberine has been found to improve glucose metabolism in type 2 diabetic patients, to operate as an important antioxidant, and to do a lot more (see “Take This Dye for Diabetes” in the November 2010 issue and “Berberine Goldthread Enhances Memory” in the April 2011 issue). To add to this story, scientific investigators are progressively reporting new findings about this natural isoquinoline alkaloid isolated from the roots, rhizomes, stems, and bark of plants such as Oregon grape, barberry, tree turmeric, amur cork tree and Chinese goldthread.

Berberine improves fasting blood
glucose by direct inhibition of
gluconeogenesis in the liver.

Berberine mechanisms that have been identified involve activation of AMPK (adenosine monophosphate-activated protein kinase) along with the improvement of fatty acid oxidation. Berberine may improve insulin sensitivity through the AMPK pathway (AMPK is a master regulator of cellular energy homeostasis) or through the induction of insulin receptor expression. However, it is not clear if berberine reduces blood glucose through some other mechanism.

In a new study, Chinese researchers addressed this issue by examining the liver response to berberine in diabetic rats, in which hyperglycemia was induced by a high-fat diet.7 In previous work, the same authors had reported that AMPK activation by berberine is dependent on mitochondrial inhibition. In their new paper, the Chinese researchers observed that berberine decreased fasting glucose significantly. Gluconeogenic genes (genes that govern the synthesis of glucose from molecules that are not carbohydrates, such as amino and fatty acids) were decreased in the liver by berberine. Hepatic steatosis (aka fatty liver disease) was also reduced by berberine and the expression of fatty acid synthase was inhibited in the liver.

Not to be dismissed, activities of transcription factors including Forkhead transcription factor O1 (FoxO1*), sterol regulatory element-binding protein 1c (SREBP1) and carbohydrate responsive element-binding protein (ChREBP) were decreased. Insulin signaling pathway was not altered in the liver. In cultured liver cells, berberine inhibited oxygen consumption and reduced intracellular adenosine triphosphate (ATP) level. When considered together, this suggest that berberine improves fasting blood glucose by direct inhibition of gluconeogenesis in the liver, an activity not dependent on insulin action. Importantly, gluconeogenic inhibition probably results from mitochondria inhibition by berberine, as suggested earlier by previous work. This observation supports the idea that berberine improves glucose metabolism through an insulin-independent pathway.

* Forkhead transcription factors are key players in development and metabolism. They regulate the expression of genes involved in cell growth, proliferation, differentiation, and longevity.

† SREBPs are transcription factors that bind to the sterol regulatory element DNA sequence TCACNCCAC. They represent complex mechanisms by which animal cells maintain the proper levels of intracellular lipids (fats and oils) in the face of widely varying circumstances (lipid homeostasis).

‡ ChREBP is activated in response to high glucose and up-regulates these genes. Cyclic AMP and a high fat diet inhibit ChREBP and slow down glucose utilization. ChREBP is able to control transcription of lipogenic enzyme genes in response to nutritional and hormonal inputs, and may play an important role in disease states such as diabetes, obesity, and hypertension.

Better to Do It All

There are many avenues by which one can work to maintain proper metabolic function and help defeat the decline into what may appear to be predictable, type 2 diabetes. Of course, lifestyle changes should be on everyone’s top list of resolutions, but by all means, make room for the judicial supplementation with vitamin E, α-lipoic acid, cinnamon, mulberry, and berberine. Your health may depend on it!


  2. Centers for Disease Control and Prevention (CDC).CDC grand rounds: childhood obesity in the United States. MMWR Morb Mortal Wkly Rep 2011 Jan 21;60(2):42-6.
  4. Patel J, Matnor NA, Iyer A, Brown L.A Regenerative antioxidant protocol of vitamin E and α-lipoic ameliorates cardiovascular and metabolic changes in fructose-fed rats. Evid Based Complement Alternat Med 2011;2011:120801.
  5. Akilen R, Tsiami A, Devendra D, Robinson N. Glycated haemoglobin and blood pressure-lowering effect of cinnamon in multi-ethnic Type 2 diabetic patients in the UK: a randomized, placebo-controlled, double-blind clinical trial. Diabet Med 2010 Oct;27(10):1159-67.
  6. Kwon HJ, Chung JY, Kim JY, Kwon O. Comparison of 1-deoxynojirimycin and aqueous mulberry leaf extract with emphasis on postprandial hypoglycemic effects: in vivo and in vitro studies. J Agric Food Chem 2011 Mar 3. [Epub ahead of print]
  7. Xia X, Yan J, Shen Y, Tang K, Yin J, Zhang Y, Yang D, Liang H, Ye J, Weng J. Berberine improves glucose metabolism in diabetic rats by inhibition of hepatic gluconeogenesis PLoS One 2011 Feb 3;6(2):e16556.

Will Block is the publisher and editorial director of Life Enhancement magazine.

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