It’s all in your Feet, Forks, Fingers, Sleep, Stress and most of all the ways you love
David Katz MD, MPH, FACPM, FACP Director, Prevention Research Center at Yale University School of Public Health has condensed sound research on lifestyle interventions to 6 domains essential to a healthy lifestyle in a pithy mnemonic he calls “feet (exercise), fork (nutrition), fingers (smoking), sleep, stress and love (Katz, Freidman & Lucan, 2015). As a strong proponent of Lifestyle as medicine Katz like many others find that lifestyle factors associated to morbidity are less about the “impact of single factors” and much more about the cumulative effect of nutrition, exercise, recreational substance use, sleep, stress and love than any one single factor (Loef and Walach, 2012). All combined, these 6 essential lifestyle factors are associated with the risk of developing major non-communicable diseases and are identified by the World Health Organization as lifestyle activities which decisively determine those who do or do not contract preventable diseases (Katz, Freidman & Lucan, 2015).
Agreed, who is going to stand up and argue with Katz? Numbers don’t lie, he’s clearly right. So what’s new? We’re still left knowing what we should do, but we just can’t quite figure out how to do it. These healthy lifestyle domains just aren’t that easy to put into practice day in and day out. We’ve got hectic lives. Since we know the answer lies in the way we eat, how much we move, whether we smoke, drink or use recreational drugs, how restful, uninterrupted and restorative our sleep, how our feelings of love or isolation make us feel and how we manage daily stress that really matters. The question is how do we accomplish all of this each and every day? If Dr Katz were here answering the question he might say something like, this kind of behavior change involves actually practicing “lifestyle as our medicine” (Katz, 2015).
Just as preventative medicine concerns how health care professionals prevent, interrupt, or relieve the impairments caused by symptomatic disease, lifestyle medicine seeks to promote patient’s proactive and self-directed health activities for establishing and maintaining wellness. Patients learn the first line of defense is their own behavioral health change rather than passively depending on medical intervention to compensate for their own unhealthy activities (Katz, et al 2014). The real clincher for Behavioral Health Clinicians (BHC) is these healthy behaviors not only form our body’s building blocks for health but our emotional and cognitive building blocks for sound minds. Feet, forks, fingers, sleep, stress and love also help regulate how we think and the way we feel (Katz, 2015).
Is Alzheimer’s disease Really Diabetes 3?
Since I am neither a neuroscientist nor an endocrinologist let me appeal to our shared common sense here that makes a pretty plausible leap in a laymans answer to this question. Although the incidence of both Alzheimer’s disease (AD) and diabetes are well established as two highly prevalent pathological conditions often found comorbid in Western society, until recently the etiological connection establishing one as following the other has more recently stirred considerable interest (Katz, et al, 2014). The idea that long-term poorly managed glucose intolerance may actually cause not just temporary delirium but progressive and irreversible vascular dementias is increasingly becoming well supported (Accardi, et al, 2012). Studies attempting to establish the link between metabolic health and cognitive performance are now referred to with terms such as “Diabetes 3” and “metabolic cognitive syndrome” (Frisardi et al, 2010).
Another case in point is a cluster of conditions which together are called Metabolic Syndrome. There is growing epidemiological support which suggests that a major disabling effect of this cluster of troubling biomarkers may be cognitive impairment (Frisardi et al, 2010). The symptomatic components of Metabolic-Cognitive Syndrome are multifactorial involving: Impaired glucose tolerance, abdominal or central obesity, hypertension, hypertriglyceridemia and reduced high-density lipoprotein cholesterol which together are also associated with age-related cognitive decline (ARCD), Alzheimer’s disease (AD) and vascular dementia. Lifestyle-related factors such as physical activity, adherence to a Mediterranean-type diet, non-smoking, “dosed” wine consumption, are also associated with prevention of dementia and pre-dementia syndromes (Solfrizzi et al., 2004).
So this growing biochemical evidence supports a tangible connection between AD as a fundamentally metabolic disease in both its molecular and biochemical pathophysiological features which relatedly also corresponds with symptoms of diabetes mellitus and other insulin resistant disorders (Accardi, 2012; De la monte, 2012). One meta-analysis of metabolic syndrome, diabetes and AD, found three biochemical mechanisms suggesting the connection between these conditions involving: (1) Systematic insulin resistant diseases linked to obesity, type 2 diabetes and non-alcoholic steatohepatitis which all promote neurodegeneration; (2) the neurodegenerative pathway is mediated by endogenous or primary brain insulin resistance which results in neuronal, energy metabolism and membrane integrity impairments and; (3) these common processes all result in cell death, myelin degeneration, and neuro-inflammation (De la Monte, 2012).
According to Katz, Freidman and Lucan (2015) the connection between type 3 diabetes and AD is more plausible as it relates to both conditions associated with lifestyle habits (nutrition, exercise and substance use) which is proven to directly impact how the brain uses glucose as energy and further how insulin resistance and insulin deficiency can cause acute delirium and related temporary cognitive slowing. Essentially, like all other homeostatic processes regulating other cells of the body, the brain’s neurons also become “starved” of glucose overtime in the presence of poorly managed diabetes (Frisardi et al, 2010). Given that the brain’s neurogenesis is dependent on glucose as its primary source of energy to recover, repair and regenerate neural functioning, it makes sense that some kind of dementia would result from long-term insulin resistance (Yaffe et al, 20014).
So although diabetes 2 itself was never before thought to impact the brain to actually cause dementia, our current understanding does implicate metabolic dysfunction as a major contributing pathogenesis or exacerbation of AD progression (de la Monte, 2013). What complicates this AD etiology and nomenclature is that metabolic disease can appear as secondary to many conditions such as obesity and non-alcoholic fatty liver disease. What is critical here for lifestyle intervention is epidemiological theory suggests that insulin resistance diseases, including AD, are “exposure related in etiology” rather than purely endogenous and therefore highly conducive to lifestyle changes.
In case you were waiting for some good news . . . you just read it. The good news is that healthy behavior change presents viable “opportunities to discover and implement new treatments and devise preventive measures to conquer AD and other insulin resistance disease” (de la Monte, 2013). Further, behavioral interventions such as feet, forks, fingers, sleep, stress and love are lifestyle habits that are the best medicine to protect our brains from dementia.
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