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a ketone-producing, lower-carbohydrate diet  that the brain is struggling to fuel itself. Unfortunately, in the absence of
          would still allow for consumption of a wide ar-  clear signs of glucose dysregulation (hypo- or hyperglycemia, obesity,
          ray of low glycemic load vegetables and fruits,  etc.), people have no reason to suspect something metabolically insidious
          which are typically richer in micronutrients,  is occurring. Therefore, regular monitoring of pertinent markers—such
          antioxidants, and phytochemicals than their  as fasting blood glucose, fasting insulin, triglycerides, and especially
          high glycemic load refined grain and sugar  HbA1c—might be the only strategy for early detection.
          counterparts.  This would make this primary     In cases of AD detected only after cognitive function has deteriorated
                     54
          avenue for therapy more practical, since the  to the point of interfering with daily life, drastic interventions such as
          difficulty with sticking to classical ketogenic  ketogenic diets and supraphysiologic doses of helpful nutrients might be
          diets is typically that they’re unpalatable and too  warranted. These are avenues ripe for exploration in future research. Life-
          restrictive. This is also likely why much of the  long reduction of risk, however, should start early and include a diet low in
          research involving KBs as AD therapy is limited  refined sugar and carbohydrates; rich in omega-3 fatty acids (specifically
          to exogenous ketones and MCT preparations;  DHA) and naturally occurring, stable saturated fats; rich in antioxidants
          classical ketogenic diets are extremely challeng-  and phytonutrients from low-glycemic vegetables and fruits; emphasis on
          ing to maintain. There is also likely trepidation  whole, unprocessed foods, and inclusion of stress reduction and muscle-
          regarding such a high fat intake—particularly  building physical activity.
          saturated fat—despite mounting evidence even     The plethora of evidence linking hyperinsulinemia, T2D, mitochondri-
          in the medical mainstream that saturated fat  al dysfunction, and glucose dysregulation—all resulting from the refined,
          intake is not associated with increased risk for  chemically manipulated modern Western diet—to Alzheimer’s disease
          cardiovascular disease, and that reductions in  suggests that the time has come for a drastic reevaluation of across-the-
          carbohydrate intake, in fact, can improve risk for  board recommendations for entire population groups to consume low-fat
          heart disease.  Promising avenues for research  and low-cholesterol diets, which are, by default, high in carbohydrates.
                      55
          in dietary therapy for AD are hindered by an  Combined with stressful and sedentary lifestyles, and particularly when
          outdated nutritional paradigm.            complicated by cholesterol-lowering medication, this amounts to nothing
                                                    less than a blueprint for creating Alzheimer’s disease and other forms of
          FUTURE AVENUES                            neurological degeneration.
              Although the ApoE4 genotype is strongly
          associated with development of AD, no genetic  Amy Berger, MS, NTP, is a nutritionist practicing in Northern Virginia.
          heritage is a death sentence. Rather, it is the  After years spent doing "all the right things," but failing to see positive
          mismatch between this hunter-gatherer geno-  changes in her health and physique, she discovered that most of what we've
          type and a seemingly inexhaustible supply of  been taught about healthy diets is incorrect. She now dedicates her career
          inexpensive, readily obtained refined sugars and  to helping others learn about real food and return to robust health. Visit
          carbohydrates, that brings about AD in these  her website at www.tuitnutrition.com or email her at tuitnutrition@gmail.
          populations. Similarly, no genetic heritage is a  com. She is available for long-distance consultations via phone or Skype.
          free pass. Groups with other variants of the ApoE
          gene are not immune to the ravages of the modern  REFERENCES
          diet. Hyperinsulinemia is the strongest known   1.   Alzheimer’s Association. Alzheimer’s facts and figures. http://www.alz.org/alzheimers_dis-
                                                        ease_facts_and_figures.asp.
          risk factor in non-E4 carriers, and overcomes   2.   Cordain L, Eades MR, Eades MD. Hyperinsulinemic diseases of civilization: more than just
          whatever protection their genes might provide.   3.   Syndrome X. Comp Biochem Physiol A Mol Integr Physiol. 2003;136(1):95-112..
                                                        Cordain, L. Cereal grains: humanity’s double-edged sword. World Rev Nutr Diet 1999;84:19-73.
          AD is not a disease of genetics, but one of epi-  4.   Craft S and Watson GS. Insulin and neurodegenerative disease: shared and specific mechanisms.
          genetics—the influence of diet, environment,   5.   Lancet Neurol 2004;3(3):169-78.
                                                        Henderson S. High carbohydrate diets and Alzheimer’s disease. Med Hypotheses 2004; 62:689-
          and lifestyle on how genes are expressed.     700.
              That Alzheimer’s disease appears late in   6.   Seneff S, Wainwright G, and Mascitelli L. Nutrition and Alzheimer’s disease: the detrimental
                                                        role of a high carbohydrate diet. Eur J Intern Med 2011;22(2)134-40.
          life does not mean the causative cascade is not   7.   Kanoski S and Davidson T. Western diet consumption and cognitive impairment: Links to
          started decades earlier. Like other “diseases of   8.   hippocampal dysfunction and obesity. Physiol Behav 2011;103(1):59-68.
                                                        Lane R and Farlow M. Lipid homeostasis and apolipoprotein E in the development and progres-
          civilization,” AD builds slowly over time, often   sion of Alzheimer’s disease. J Lipid Res 2005;46(5):949-68.
          with no overt symptoms, until damage is already   9.   Moreira P, Santos M, Seica R, et al. Brain mitochondrial dysfunction as a link between Al-
                                                        zheimer’s disease and diabetes. J Neurol Sci 2007;257(1-2):206-14.
          widespread and, in some cases, irreversible.   10.  Mamelak M. Alzheimer’s disease, oxidative stress and gammahydroxybutyrate. Neurobiol
                                                        Aging 2007;28(9):1340-60.
          What we consider the normal forgetfulness of   11.  Reiman E, Kewei C, Alexander G, et al. Functional brain abnormalities in young adults at
          older age might very well be early warnings   genetic risk for late-onset Alzheimer's dementia. Proc Natl Acad Sci USA 2004;101(1):284-289.
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   137720_text.indd   43                                                                                       7/1/14   11:41 AM
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