weight loss study

Research proposal to formulate a dietary and exercise program to address Diabetes type 2 and Alzheimer’s in adults aged 30 to 45 working in high stress office jobs

by Hugo Allen-Stevens

The incidence of chronic disease in the United States is set to rise at an unprecedented rate. A report from the Milken Institute (2014) estimates that:

More than 109 million Americans report having at least one of the seven diseases, for a total of 162 million cases. The total impact of these diseases on the economy is $1.3 trillion annually. On our current path, in 2023 we project a 42 percent increase in cases of the seven chronic diseases and $4.2 trillion in treatment costs and lost economic output. Lower obesity rates alone could produce productivity gains of $254 billion and avoid $60 billion in treatment expenditures per year.

Obesity is also 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.

A concurrent factor is the aging of the population worldwide which will lead to an increase in diseases related to aging, such as dementia. For Alzheimer’s disease alone, a report by John Hopkins University (2007) estimates the incidence will quadruple so that by 2050, 1 in 85 persons worldwide will be living with the disease. Overall, a shift to more effective preventative treatment is needed in order to offset the rising economic and human cost both of the aging population and failure to address obesity.

This paper will address factors that affect the health of males and females working in high stress office jobs that lead to the incidence of Alzheimer’s and Diabetes type 2. The target population is of 30 to 45 years of age and a program is promoted that is intended to address factors such as stress and insulin surging that lead to enhanced incidence of these diseases as well as ineffective weight loss. Overall, this paper will therefore outline measures for further research and work on forming a health program that sustainably reduces body fat and enhances vitality and in doing so leads to reduced risk and incidence of obesity, insulin resistance, brain degeneration 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 wellbeing. 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 behaviors 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 behaviors 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.


Haltia et al. (2006) show in a 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 type 2 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. As noted in the study by Haltia (2006), tackling obesity is a key factor in modulating Alzheimer’s, as it is a key factor in other chronic diseases. It is at this point that diets that attempt to induce weight loss through aggregate calorie or carbohydrate reduction fail. It is also where exercise programs that attempt to address stress and also encourage weight loss lead to increased health problems.

Metabolic rate and inflammation

Hyman (2006) notes that calorie restricted diets trigger the body to perceive dieting as starvation periods. This in turn triggers survival patterns that lead the body to replace energy stores lost during a diet. And this energy is replaced as fat when the diet is over. Meanwhile cortisol is upregulated in order to make up for the energy deficit during calorie restriction by breaking down muscle for energy. In effect, calorie restricted diets lead to muscle loss and fat accumulation at the end of the diet and a yo-yoing of weight that prohibits sustained weight loss.

Meanwhile the release of cortisol during periods of calorie restriction place the body in a pro-inflammatory state. In the process, cortisol acts to increase inflammatory cytokines such as interleukin 6 which can enhance brain degeneration, or exacerbate demands on the immune system leading to immune hyper-sensitivity and allergies, or immune overload and illness. This may also be enhanced by endogenous or exogenous toxins, such as toxins stored in fat tissue and released during dieting.

An additional point is that when calories are restricted, the metabolic rate is lowered via downregulation of thyroid hormones . This process is noted by Ross (1999) as a way to conserve energy during what it perceives to be a famine. What is important is that the body becomes more used to being starved of its preferred fuel which typically is carbohydrate and glucose. As it does so, the body becomes conditioned to switching to energy conservation through thyroid downregulation leading to conditioned hypothyroidism. The effect of this is that the adrenals compensate to up-regulate energy supply through glycogen and muscle protein catabolism. And this pattern can contribute to adrenal fatigue, especially with a person who is already dealing with stress related to work.

Adding to this burden, hypothyroidism induced by calorie restriction also induces neurological imbalances related to dopamine and serotonin. These imbalances are noted by Braverman (2009) to lead to carbohydrate cravings to compensate for energy and neurotransmitter deficiency, as well as patterns of addiction related to behavioral attempts to induce limbic stimulation. The overall effect therefore could be a person who becomes addicted to dieting and the process of losing weight. In could also contribute to addiction to exercise.

Exercise in itself may be beneficial to health. However it may also be stressful, especially if it is raises a person to above 70% of their maximal heart rate. The key issue at this point is the burden of oxidative stress induced by exercise and the resources available for the body to cope. It is at this point that the nutritional status becomes imperative, not simply to fulfill energy demands, but also to repair exercise induced damage with key nutrients, such as anti-oxidants. The failure to do so merely adds to the burden on the body stemming from stress related factors such as work, immune status and toxin exposure. And it is factors such as these that need inclusion in the health program this paper proposes to research.

Dietary program outline

The foundation of this health program is a diet such as the Zone diet that both enhances health and avoids insulin surging that leads to sub-optimal brain and body function. Addressing foods with a high glycemic index, Sears (1995) notes that the resultant insulin surging inhibits oxygen delivery to brain and muscle tissue, in effect reducing brain and muscle function. In addition, recurrent surging derived from high carbohydrate diets conditions the body to store fat and use carbohydrate for fuel, in the process inhibiting fat loss. Sears notes that a pivotal process involved in this are inflammatory eicosannoids derived both from the diet and also from fat tissue and stress. He therefore advises a diet that places an emphasis on including an equalized balance of fat, protein and carbohydrate with particular attention to the types of macronutrients to ensure protein in bioavailable, fat is plentiful in healthy eicosannoids and high glycemic carbohydrate are avoided. These claims seem credible and warrant further research for inclusion in the health program particularly with regard to the macronutrient proportions.

Addressing these proportions, Teta and Teta (2009) subdivide people into types based upon their predominance to burn glucose or protein. These predominating factors relate to hormonal factors influenced by food choices which Teta and Teta modulate through varying carbohydrate content and type. This approach, which begins to tailor macronutrient proportions to underlying metabolic factors and body types is excellent. They also have an excellent approach to food portion sizing and timing, stressing meals at regular intervals to avoid blood sugar imbalances, and ensuring a blend of complex carbohydrate, protein and fat at all meals. However the understanding of people as “types” deserves further investigation, particularly with regard to whether and more importantly why a person may be prone to fast or slow oxidization, high or low blood acidity or parasympathetic or sympathetic nervous system dominance. These factors tie directly into factors which affect metabolic rate and metabolism and are addressed by Wolcott and Fahey (2002). Thus further research for forming specific dietary prescriptions based upon people “type” in needed.

With regard to weight reduction through exercise, Sears (1995) and Hyman (2006) emphasize an exercise intensity that increases exertion to the point where fat is catabolized, cells become sensitized to insulin and human growth hormone is released, further enhancing fat catabolism. This is added to by Teta and Teta (2009) whereby an approach based upon muscular exertion to the point of muscular failure is advocated in order to induce anabolic muscle building. This approach combines the release of myokines from muscle tissue as well as harnessing the effects of cortisol and testosterone in order to raise the metabolic rate for weight loss and fat catabolism that is sustained for up to 48 hrs after a workout. This approach, especially with regard to raising metabolic rate for fat burning is excellent. However the overall effect use of stress hormones requires careful consideration, especially with regard to the overall health status related to adrenal fatigue, toxic overload, immune dysfunction and hormonal imbalance.

To address these health factors, an individualized approach is needed to assess factors such as Progesterone induced hypo or hyperthyroidism in women. These factors are raised by Kharrazian (2009) along with the effects of stress on thyroid function as well as allergy and toxins. Overall, given the importance of the thyroid in regulating the metabolic rate and in turn fat metabolism, it is imperative thyroid health be assessed and proper thyroid support be afforded during weight loss. In addition, thyroid health and support is imperative for healthy brain function and neurotransmitter function. And this has an effect on cravings, addictions and behavior that may be needed to be modified during the diet in order for weight loss and brain health to be sustained. Equally, further consideration needs to be made with regard to brain chemistry, such as those emphasized by Ross (1999) and Braverman (2009). Specifically this relates to possible imbalances in neurotransmitters that lead to behavioral imbalances, such as food or exercise addictions.

The program that is proposed at this point aims to stress protein intake at every meal, thus including amino acids needed for optimal neurotransmitter function and brain health. It would also emphasize a low glycemic carbohydrate intake for blood sugar management, with carbohydrate sourced from vegetables and fruit to ensure fiber content again for optimal blood sugar management. Furthermore it would ensure regular timing of meals and all food types being present at all meals, and ensure sufficient fat intake especially of anti-inflammatory Omega 3 oils. Overall is would be based on the Paleo dietary approach which also appears to the underlying approach advocated by Teta and Teta (2009). What is most significant about this approach is that it combines a low toxic load with an abundance of natural foods rich in anti-oxidants and nutrients to sustain health, especially as the body is placed under strain whilst toxins from fat are removed and oxidative stress induced by exercise is increased. In addition the approach advocated by Cordain (2012) avoids most grains and legumes under the consideration that phytates, lectins, saponins and other natural biological compounds present in those foods lead to damage of the mucosal lining of the gut. This seems to be an optimal dietary approach, especially with regard to brain inflammation from allergy responses and gut permeability.

Grains meanwhile are noted by Perlmutter (2013) for also causing the highest effect on blood sugar as well as the strongest inflammatory load on the brain, especially in those people who are either intolerant or allergic to gluten. Perlmutter meanwhile advocates a ketogenic diet under the thesis that ketones provide an energy fuel for the brain that is neurogenerative. Whilst Perlmutter’s other claims regarding the effects of grain and the need for their restriction seem worthy of inclusion in a brain health and weight conscious diet, this particular claim regarding ketones deserves careful consideration and further research.


Whilst the program that could be advocated at this point would be based upon a whole foods diet with specific emphasis on anti-inflammatory foods, detoxification, blood sugar management and exercise at varying degrees of intensity, further research is needed. This research is needed for hormonal and neurochemistry management as well as how energy types, such as ketones, effect brain function. And this research is needed not simply to ensure that the program is effective, but also that it can be tailored to suit individual “types” of people and their individual states of being. Overall further research is needed to make weight loss and brain health a lifestyle and not simply a diet.


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

Chatterjee, A., et al. (2014). Chronic Disease and Wellness in America. MILKEN INSTITUTE. Retrieved from: http://www.milkeninstitute.org/publications/publications.taf?function=detail&ID=38801460&cat=save

Cordain, L. (2012). The Paleo Answer. Hoboken, N.J.: John Wiley

Cordain, L. (2002). The Paleo Diet. Hoboken, N.J.: John Wiley

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

Kharrazian, D. (2009). Why Do I Still Have Thyroid Symptoms?  New York, N.Y.: Morgan James Publishing

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

Sears, B. (1995). The Zone Diet: A Dietary Road Map. New York, NY: Harper Collins

Teta, J., Teta, K. (2009). The New ME Diet. New York, NY: Harper Collins

Wolcott, W. and Fahey, T. (2002). The Metabolic Typing Diet. New York, N.Y.: Broadway

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