Diabetes and obesity are global health conditions which are increasing. Adult obesity prevalence increased from 13 to 32% between the 1960s and 2004. Changes in obesity prevalence among children and teens tripled, from nearly 5% to approximately 15% since the 1960s. Currently, 66% of U.S. adults are overweight or obese. The incidence of diabetes is increasing and a icting new populations including children and developing societies. Diabetes is occurring at younger ages and at lower BMI levels . It appears that both our understanding of the disease and our treatment of the disease are inadequate. Current approaches are not working.
Current disease model
It is widely believed that overeating calorie-dense food, particularly a high-fat diet, together with an inactive lifestyle causes obesity. With increased fat, the β-cells of the pancreas increase insulin production in order to store fat without causing hypoglycemia. Eventually the beta cells wear out and are not able to maintain su ciently elevated insulin levels.
The current standard treatment for diabetes includes diet, exercise, and medications that increase circulating insulin.
The time has come to extend the model of diabetes to include the environmental changes that have accompanied the epidemics of obesity and diabetes. Diabetes is not only caused by obesity. Only forty percent of the risk for developing diabetes occurs in people who are obese The chemicals in our food, environment and the use of drugs in our food animals
and the processing and packaging of our foods have increased the toxins in the environment. These toxins in our environment and diet can lead to a leaky gut, inflammation, oxidative stress and mitochondrial dysfunction.
THE ROLE OF GUT MICROBIOTA
Gut microbiota plays a significant role in the development of obesity, obesity-associated inflammation and insulin resistance (Shen et al. 2013) and in diabetes and non alcoholic fatty liver disease (Delzenne et al. 2011) and autoimmune diabetes such as found in diabetes type I and diabetes 1.5 (LADA) (Vaarala 2010).
The gut microbiota in adults with type 2 diabetes di ers from that in non diabetic adults (Larsen et al. 2010). The gut may modulate the influence of life style events triggering the development of type 2 diabetes (Allin et al. 2015).
and can cause symptoms of the metabolic syndrome (Koren et al. 2012) and serum glucose levels (Larsen et al 2010). Toxins from some strains of bacteria Staph aureus scan cause diabetes
(Vu et al. 2015)
FACTORS LEADING TO INSULIN RESISTANCE
Sleep deprivation may lead to insulin resistance and subsequently to diabetes mellitus (Albal, Bahammam 2011)
Toxins such as phthalates. In addition to sleeping problems, tress, depression, anxiety, anger, and hostility are associated with an increased risk for the development of type 2 diabetes (Pouwer et al. 2010).
THE ROLE OF TOXINS
Toxins can lead to diabetes by
- Interferingwithglucoseandcholesterol metabolism inducing insulin resistance
- Impairingappetiteregulation Toxins associated with diabetes include:
• Phthalatesarelinkedtomarkersofglucose tolerance and insulin resistance (Dirinck et al. 2015). Phthalates are found in plastics and cosmetics, flame retardants and pesticides (Lind et al. 2012).
- BisphenolA(BPA)foundinfoodcanliningsand cash register receipts (Gore et al, 2015)
- Heavymetalssuchasarsenic,iron,mercury, lead, cadmium and nickel (Gonzalez-Villalava et al. 2016)
- PolychlorinatedBiphenylsandDioxins(Wanget al. 2008). There is a causative association between polychlorinated biphenyl (PCB) exposure and obesity-induced insulin resistance and hyperinsulinemia independent of body weight (Gray et al. 2013).
- PersistentOrganicPollutants(POPs)suchas organochlorine pesticides exposure leads to insulin resistance and associated metabolic disorders (Ru n et al. 2010). Diabetes prevalence was strongly positively associated with lipid- adjusted serum concentrations of at least six POPs (Lee et al. 2006).
Statins, second generation antipsychotics havebeen associated with an increased risk of diabetes.Food additives (Helgason, Jonasson, 1981) and zinc, magnesium and chromium deficiencies (Gonzalez- Villalava et al. 2016) have adverse e ects on glycemic control.
RECOMMENDED LABORATORY EVALUTATIONS
Fasting insulin and 30 minutes after 75 g glucose and 2 hour levels are recommended to assess serum glucose levels and insulin sensitivity. Measuring insulin 30 minutes after a meal is a good measure of insulin secretion (Ludwig et al. 2008). Somprehensive stool analysis to assess gut pathogenic bacteria, fungi, parasites
- Treatgutissuesincludingprebioticsand probiotics
- Minimizetoxinexposureandgentledetoxsuchas Epsom salt baths, saunas. Supplements to support liver detoxification include (Kresser 2010)
o Protective compounds like milk thistle and artichoke leaf extract
o Bile stimulants such as dandelion and curcumin
o Bile motility enhancers (cholagogues) like dandelion, beet juice and co ee enemas
o Antioxidants like vitamins C & E, zinc, selenium and lipoic acid
• Healthyorganic,nonprocessedfooddietwith grass fed meats and wild fish.
o No GMOs or high fructose corn syrup
o Minimize sugar consumption
o Caloric restriction can improve beta cell function, improve insulin sensitivity (Cho, 2014)
o High fiber
- Nutrientstomodifyinsulinresponsivenessatthecellular level including
o Chromium, alpha lipoic acid, co enzyme Q 10, vitamin D, Magnesium, vitamin C, Vitamin E and other antioxidants
o Omega 3 fatty acids o Vanadium
mpounds that support health liver detoxification include:
• Protective compounds like milk thistle and artichoke leaf extract
- Bile stimulants such as dandelion and curcumin
- Bile motility enahncers (cholagogues) like dandelion, beet juice and co ee enemas
- Antioxidants like vitamins C & E, zinc, selenium and lipoic acidREFERENCES
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