Type 2 diabetes is the archetypal lifestyle disease, a metabolic dysfunction run out of control to the point at which it disrupts the crucial mechanisms of insulin metabolism. Diabetes isn't accelerated aging, but it has many of the same consequences when viewed from the high level: more damage, more disease, higher mortality. The vast majority of type 2 diabetics have this condition as a result of the choices they made. It is easy to become fat in a world of low-cost calories and increasing wealth, but it is still a choice. We can turn a questioning eye to Alzheimer's disease, a progressive age-related dementia characterized by a range of changes in the biochemistry of the brain, such as amyloid and tau deposits, and ask to what degree it is a lifestyle condition, driven by visceral fat tissue, lack of exercise, and the like. When looking at lifestyle choices and risk, the answers are more ambiguous than is the case for type 2 diabetes, however. Consider cardiovascular disease, for example. You can lead a life that makes you much more likely to die young from a heart attack, but equally everyone will suffer cardiovascular failure if they live long enough - the processes that weaken the heart and corrode our blood vessels operate in everyone, just more rapidly in the obese.
Is Alzheimer's more like type 2 diabetes, 90% avoidable over a normal human life span for the diligent, or is it more like cardiovascular disease, inevitable for all of us, absent radical progress in medical science, but arriving sooner for the less diligent? You'll see arguments either way if you wander the literature, most of which lean in the direction of Alzheimer's as a lifestyle condition, but not to the same degree as type 2 diabetes. A good meta-analysis from last year puts some numbers to that summary: if nine-tenths of type 2 diabetes is self-inflicted, then one can argue for two-thirds of Alzheimer's to be self-inflicted by the same types of statistical approach. Being overweight is definitely on the list: the distortions of metabolism caused by excess visceral fat tissue impact the brain. There is even a faction within the research community who argue that Alzheimer's is a type 3 diabetes, in effect.
Perhaps a better measure of the degree to which a medical condition is a lifestyle condition is whether or not it can be effectively treated, reversed, or cured by lifestyle changes alone. This is the case for type 2 diabetes. Even fairly late in its progression, calorie restriction and consequent loss of fat tissue can turn things around for a majority of patients, to the point of a cure. It is somewhat amazing that so many people continue down the road of disability when they could turn back at any time. For cardiovascular disease, lifestyle interventions like increased regular moderate exercise are beneficial, but in the way of a delaying tactic. You can improve the present poor situation, but you can't choose your way to back to full health for your age given the tools available. When it comes to the option to turn back, is Alzheimer's disease more like type 2 diabetes or more like cardiovascular disease, once it has taken hold?
The publicity materials and paper I'll point out today add a little more data from a small set of patients to the present evidence on this topic, putting Alzheimer's more in line with what one might expect from comparing the risk factors. Note the date on the paper, two years ago, versus the date on the publicity, however, this week. These results have been languishing for a few years, and by the look of it the researchers involved are now attempting another angle to broaden support for their approach - whenever book publication is mentioned in a release, it's a fair guess that the forthcoming book is why the release exists. Pitching a strategy of lifestyle changes to the usual panoply of research funding sources has ever had the problem that lifestyle changes are a poor foundation for a for-profit business, and are in any case well outside the area of interest for most for-profit funding sources relevant to medical research. It took some years for the calorie restriction research community to figure out a way to get for-profit interests involved, for example. That sort of challenge may well be what is taking place behind the scenes here, but equally it could simply be a mundane case of business failure for reasons unrelated to the science.
Results from quantitative MRI and neuropsychological testing show unprecedented improvements in ten patients with early Alzheimer's disease (AD) or its precursors following treatment with a programmatic and personalized therapy dubbed metabolic enhancement for neurodegeneration (MEND). The study is the first to objectively show that memory loss in patients can be reversed, and improvement sustained, using a complex, 36-point therapeutic personalized program that involves comprehensive changes in diet, brain stimulation, exercise, optimization of sleep, specific pharmaceuticals and vitamins, and multiple additional steps that affect brain chemistry. "All of these patients had either well-defined mild cognitive impairment (MCI), subjective cognitive impairment (SCI) or had been diagnosed with Alzheimer's disease before beginning the program. Follow up testing showed some of the patients going from abnormal to normal."
All but one of the ten patients included in the study are at genetic risk for AD, carrying at least one copy of the APOE4 allele. Five of the patients carry two copies of APOE4 which gives them a 10-12 fold increased risk of developing AD. "We're entering a new era. The old advice was to avoid testing for APOE because there was nothing that could be done about it. Now we're recommending that people find out their genetic status as early as possible so they can go on prevention." Sixty-five percent of the Alzheimer's cases in this country involve APOE4; with seven million people carrying two copies of the ApoE4 allele. "The magnitude of improvement in these ten patients is unprecedented, providing additional objective evidence that this programmatic approach to cognitive decline is highly effective. Even though we see the far-reaching implications of this success, we also realize that this is a very small study that needs to be replicated in larger numbers at various sites."
Effective treatment of Alzheimer's disease has been lacking, but recently a novel programmatic approach involving metabolic enhancement was described, with promising anecdotal results. This treatment is based on connectomic studies and previous transgenic findings as well as epidemiological studies of various monotherapeutic components of the overall program. The approach is personalized, responsive to suboptimal metabolic parameters that reflect a network imbalance in synaptic establishment and maintenance vs. reorganization, and progressive in that continued optimization is sought through iterative treatment and metabolic characterization.
Here we report the initial follow-up of ten patients who were treated with this metabolic programmatics approach. One patient had well documented mild cognitive impairment (MCI), with a strongly positive amyloid-PET (positron emission tomography) scan, positive FDG-PET scan (fluorodeoxyglucose PET scan), abnormal neuropsychological testing, and hippocampal volume reduced to 17th percentile; after 10 months on the MEND protocol, his hippocampal volume had increased to 75th percentile, in association with a reversal of cognitive decline. Another patient had well documented early Alzheimer's disease, with a positive FDG-PET scan and markedly abnormal neuro-psychological testing. After 22 months on the MEND protocol, he showed marked improvement in his neuropsychological testing, with some improvements reaching three standard deviations from his earlier testing.
The initial results for these patients show greater improvements than have been reported for other patients treated for Alzheimer's disease. The results provide further support for the suggestion that such a comprehensive approach to treat early Alzheimer's disease and its precursors, MCI and SCI, is effective. The results also support the need for a large-scale, personalized clinical trial using this protocol.