In part one we introduced lyme disease and discussed how it can include many more infections over and above Borrelia burgdorferi (BB). In part two we will explore what makes tick-born infections so poorly understood and hard to diagnosis. Narrow Definition: The Center for Disease Control (CDC) and Infectious Disease Society of America have restricted the definition of “lyme disease” to only the acute stage of lyme where the “bulls eye” rash (note: this occurs in less than 30% of cases) is present and the patient is experiencing “flu-like” symptoms. This discounts all the patients with persistent symptoms which
It is clear that a diet high in fructose can predispose a person to multiple disease processes. Figure Two here summarizes the effects of fructose and the connection with type 2 diabetes.
The ability of fructose to raise uric acid levels sheds some light on possible mechanisms in the development of diabetes and metabolic syndrome. This may be a new area where early interventions can be used. In animal and human trials, lowering uric acid improved a number of features of metabolic syndrome, which include renal damage, insulin resistance, high triglycerides and hypertension (Nakagawa et al 2006). It seems that fructose induced damage via uric acid may be a key initiating factor in the cascade of progression in metabolic syndrome since it drives may underlying processes.
The harmful effects of fructose make it clear that reducing intake it a key part of any chronic disease prevention or treatment plan. The most important thing would be to reduce intake from refined foods and drinks such as soft drinks, juices, and candy. Even though fruit contains fructose, ingestion has not been associated with the development of diabetes while fruit juices (added HFCS) have been. Whole fruit contains other nutrients such as fibre and antioxidants that have a protective effect against the damage of fructose (Bazzano et al 2008).
Gout, which is the most well known effect of high levels of uric acid, is a known risk factor for type 2 diabetes (Saggiani et al 1996). Also considering the effect of a diet high in refined sugar and the production of uric acid, measures should be employed to reduce uric acid levels in both gout patients and also diabetics (especially pre-diabetics). This may be a missing link in the progression and initiation of diabetes.
What I find even more interesting is that Mulberry leaf has been herb remedy traditionally used in Chinese medicine to treat diabetes. Research trials have confirmed that mulberry has the ability to reduce insulin resistance (Tanabe et al 2011). Other animal trials have also shown that mulberry leaf has antioxidant, anti-hypertensive, and anti-inflammatory effects. Recent research has also shown that morin, a compound found in mulberry leaf, is a potent xanthine oxidase inhibitor and inhibitor of renal urate reabsorption (Yu Z, et al 2006). The dual in functions peaked my interest as a novel intervention for both diabetes and gout. There is evidence that xanthine oxidase inhibitors can prevent the development of metabolic syndrome induced by fructose (Nakagawa et al 2006). This shows promise for the use of mulberry leaf as an early diabetes and metabolic syndrome intervention.
In addition to reducing your intake of HFCS, sucrose and fructose, someone with metabolic syndrome and a risk for developing type 2 diabetes should reduce their uric acid levels. To reduce the levels, one should also reduce the intake of purine rich foods such as meats and shellfish, which are converted to uric acid. Alcohol, especially beer, can also raise uric acid. Vitamin C has multiple actions to prevent the negative effects of uric acid. It can lower levels by promoting excretion and it can protect against the harmful effects of fructose at the cellular level (Johnson et al, Gao et al, Huang et al. 2008). Through dietary changes, adequate intake of antioxidants and a herbal extract such as mulberry we may be able to effectively tackle the a new underlying process that may be driving diabetes. For more information about the role of fructose, uric acid and diabetes please refer here to the well-written paper by Johnson et al 2009.
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Yu Z, et al. The dual actions of morin (3,5,7,2′,4′-pentahydroxyflavone) as a hypouricemic agent: uricosuric effect and xanthine oxidase inhibitory activity. J Pharmacol Exp Ther. 2006 Jan;316(1):169-75
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