Here in this post I give an outline of the study paper I wrote regarding a plan for weight loss. In it I map out the link between Type 2 Diabetes and Alzheimer’s – which is giving rise to the term Diabetes Type 3.
A report by John Hopkins University (Brookmeyer, R., et al., 2007) estimates the incidence of Alzheimer’s disease will quadruple so that by 2050, 1 in 85 persons worldwide will be living with the disease. And noted in a study by Haltia (2006), tackling obesity is a key factor in modulating Alzheimer’s. Underlying this is a causal link between obesity and Alzheimer’s – Diabetes Type 3.
Haltia et al. (2006) show in their study that obesity leads to increased incidence of white matter legions in the brain. Conversely these legions associated with Alzheimer’s decreased with dieting and weight loss. Braverman (2009) commenting on the study associates the legions with insulin resistance and low levels of acetylcholine in the brain linked to the loss of insulin-like growth factor function. Braverman also points out that insulin is produced in the hippocampus, the area where acetylcholine is most active and where damage associated with Alzheimer’s occurs. In effect, loss of sensitivity in this area to insulin leads to decreased growth promoted by insulin as well as decreased delivery of glucose and energy by insulin. In effect, brain cells are starved by lack of insulin or lack of sensitivity to it, and starved of stimulation by acetylcholine. These factors contribute to neuronal degeneration and death.
This association between insulin resistance and Alzheimer’s is known as Diabetes Type 3. The physiological mechanisms behind this association is further elucidated by Perlmutter (2013) as the body’s inability to break down neuronal amyloid plaque due to insulin resistance. This may be caused by the lack of cellular functionality that insulin sensitivity promotes, such as the growth and energy delivery alluded to above. It can also be explained by the oxidative damage caused by the increased circulation of glucose that insulin resistance causes. This oxidative damage couples with increased glycation of both lipids and proteins and also increased inflammatory responses. These responses lead to direct damage to brain cells and also arterial damage and blockages that lead to reduced oxygen delivery and neuronal ischemia.
In effect, Alzheimer’s and Diabetes have direct links to blood sugar surges and insulin surges. These surges may be caused by stress or by dietary intake of simple carbohydrates. Meanwhile chronic stress and excess cortisol has links to neuronal damage, sarcopenia and fat accumulation which in turn has leads to Alzheimer’s and Diabetes.
Stress and insulin surging
Sapolsky (2004) notes that stress causes damage to the hippocampus through neuronal damage that further promotes the incidence of Alzheimer’s disease. Principally this occurs due to the excitory effects of glucocorticoids such as cortisol on neurons, as well as impaired glucose and oxygen delivery to the brain when the stressor is prolonged or chronic. In addition, stress hormones such as cortisol lead to surges in blood sugar which promote inflammatory cytokines which, in the brain, further promote brain degeneration as well as insulin surging.
Related to chronic stress, Kharrazzian (2013) notes how a person may develop a conditioned brain response to stress, or neuroplasticity, so that key areas of the brain become more effective at responding to stress. This is turn causes an upregulation of inflammatory cytokines such as IL-6 which promote brain degeneration. Meanwhile stress promotes a downregulation of areas of the brain that regulate the nervous system and digestion, whilst brain degeneration affects the brain’s communication to the gut via the vagus nerve further impairing digestive function. In effect, gut permeability may be triggered by the increased inflammation, the brain degeneration or the impaired digestive function promoted by stress. This gut permeability and inflammation leads to increased brain inflammation and increased brain microglial activity which leads to impaired mental function and increased brain degeneration. And these factors lead to increased incidence of Alzheimer’s.
Insulin surging is meanwhile noted by Kharrazzian (2013) for promoting tryptophan uptake by the brain. This uptake promotes serotonin production which can promote feelings of well being. This, combined with the rapid rise on blood glucose and rush of energy promoted by high energy foods or the release of stress hormones explains how people may form addictions to behaviours through insulin surging and serotonin uptake. Overall a person may not only become more conditioned and effective at responding to stress, but also more addicted to unhealthy behaviours and poor food choices and in turn more prone to both a leaky gut and an inflamed and degenerating brain.
Insulin surging in itself also promotes fat accumulation. Together with the catabolic effects on muscle tissue of cortisol released due to chronic stress, these factors combine to reduce lean body mass and increased adipose tissue. This adipose tissue also releases inflammatory cytokines that contribute to neuronal damage and Alzheimer’s. In addition, other biological compounds released by adipose tissue place the body in a state of both fat conservation and fat accumulation through the negation of fat being used as a source of fuel for the body. This process, promoted by a diet rich in simple carbohydrates, further conditions the body to use carbohydrates for fuel and also promotes insulin surging and fat accumulation. The net result of this process leads to insulin resistance, diabetes and obesity.
Obesity is meanwhile noted by Hyman (2006) as being the key underlying factor in disease states such as heart disease, stroke, cancer, dementia and diabetes. In effect, addressing and preventing obesity could be the most important step toward lowering the incidence of the most common disease states. However whilst obesity is noted by Hyman to affect over 60% of the adult population and leading to a reduction in life expectancy of up to 13 years, only 2 to 6% of diets are reported as being successful in sustaining weight loss.
Whilst obesity as such may be observed as the cause of common diseases, it is in fact the chronic state of inflammation, insulin resistance and insulin surging that form the root causes (amongst others). As noted above, stress and dietary problems (such as carbohydrate addiction) play a key role as well. And involved in this are hormonal factors relating to the adrenal hormones (such as cortisol). To address this, a new approach to dieting is needed.
The focus of this approach is on lifestyle intervention and hormonal modulation to ensure insulin and adrenal health. It would involve measures inside dietary and exercise routines that promote optimal function of both hormones and neurotransmitters. This should also include measures to ensure weight loss is sustained through emphasis on thyroid health and overall metabolic rate. Further details about this proposal can be found in my study posted here.
Braverman, E. (2009). Younger (Thinner) You Diet. New York, N.Y.:Rodale.
Brookmeyer, R., et al. (2007). Forecasting the Global Burden of Alzheimer’s Disease. Alzheimer’s and Dementia 3.3 (2007): 186-191. Retrieved from: http://works.bepress.com/rbrookmeyer/23
Haltia, L.T., Viljanen, A., et al. (2006). Brain White Matter Expansion in Human Obesity and the Recovering Effect of Dieting. Journal of Clinical Endocrinology & Metabolism, 92 (8), 3278–3284. doi: 10.1210/jc.2006-2495
Hyman, M. (2006). Ultrametabolism. New York. N.Y.: Scribner
Kharrazian, D. (2013). Why Isn’t My Brain Working? Carlsbad, C.A.: Elephant Press
Perlmutter, D. (2013). Grain Brain. New York, N.Y.: Little, Brown and Company
Ross, J. (1999). The Diet Cure. New York, N.Y.: Penguin
Sapolsky, R.M. (1994). Why Zebras Don’t Get Ulcers. NewYork, N.Y.: Owl Books