Dr. Craig Reese, DC. PC.

3000 Center Green Dr. Suite 230
Boulder, CO 80301

Dr. Reese’s Bits and Pieces
September 2015 Newsletter

It’s hard to believe that fall will start this month.  I know it’s not a shock to the kids who are already back in school.  For many, fall is the time of the year to make positive changes to their lives and lifestyle.  Maybe it’s because they had way too much fun during the summer?  New research has again proven that lifestyle changes and supplements can do things that no drug can match.

Cognitive Decline
This is a subject that a lot of people joke about (“having a senior moment”) but is becoming a serious problem in this country.  The Journal of Aging had an article about this last August.  Part of the article states:

Magnitude of the problem
Cognitive decline is a major concern of the aging population, and Alzheimer's disease is the major cause of age-related cognitive decline, with approximately 5.4 million American patients and 30 million affected globally [1]. In the absence of effective prevention and treatment, the prospects for the future are of great concern, with 13 million Americans and 160 million globally projected for 2050, leading to potential bankruptcy of the Medicare system. Unlike several other chronic illnesses, Alzheimer's disease prevalence is on the rise, which makes the need to develop effective prevention and treatment increasingly pressing. Recent estimates suggest that AD has become the third leading cause of death in the United States [2], behind cardiovascular disease and cancer. Furthermore, it has been pointed out recently that women are at the epicenter of the Alzheimer's epidemic, with 65% of patients and 60% of caregivers being women [3]. Indeed, a woman's chance of developing AD is now greater than her chance of developing breast cancer [4]. (http://www.impactaging.com/papers/v6/n9/full/100690.html)

Failure of monotherapeutics

Neurodegenerative disease therapeutics has been, arguably, the field of greatest failure of biomedical therapeutics development. Patients with acute illnesses such as infectious diseases, or with other chronic illnesses, such as cardiovascular disease, osteoporosis, human immunodeficiency virus infection, and even cancer, have access to more effective therapeutic options than do patients with AD or other neurodegenerative diseases such as Lewy body dementia, frontotemporal lobar degeneration, and amyotrophic lateral sclerosis. In the case of Alzheimer's disease, there is not a single therapeutic that exerts anything beyond a marginal, unsustained symptomatic effect, with little or no effect on disease progression. Furthermore, in the past decade alone, hundreds of clinical trials have been conducted for AD, at an aggregate cost of billions of dollars, without success. This has led some to question whether the approach taken to drug development for AD is an optimal one.

Time for a New Model
The drug cure model has proven to be a failure so they looked at models used to help treat other chronic diseases like osteoporosis:

Based on a combination of in vitro and in vivo studies, we have advanced a model in which AD results from an imbalance in endogenous plasticity signaling (Fig. 1), [5-9], and in which the β-amyloid precursor protein (APP) is a mediator of such plasticity-related signaling. Thus the model suggests that AD is analogous to other chronic illnesses such as cancer, osteoporosis, and atherosclerosis. In the case of osteoporosis, osteoblastic signaling is chronically exceeded by osteoclastic signaling, resulting in an age-associated chronic illness featuring loss of bone. By analogy, in Alzheimer's disease, there is a fundamental, age-associated imbalance between the dynamically opposed physiological processes that mediate plasticity, i.e., between synaptoblastic and synaptoclastic activity.

In English, they are saying that there are nerve synapse destroying processes and synapse building processes.  Their treatment model works to support the synapse building and inhibit the synapse destroying lifestyle choices that successfully reversed the cognitive decline of 9 out of 10 patients they treated.  The 10th was in end-stage Alzheimer’s disease and didn’t get better.  There is always a “point of no return” if you let things progress too far.  The factors they tried to control are listed in the table below:
Table 1. Therapeutic System 1.0



Rationale and References

Optimize diet: minimize simple CHO, minimize inflammation.

Patients given choice of several low glycemic, low inflammatory, low grain diets.

Minimize inflammation, minimize insulin resistance.

Enhance autophagy, ketogenesis

Fast 12 hr each night, including 3 hr prior to bedtime.

Reduce insulin levels, reduce Aβ.

Reduce stress

Personalized—yoga or meditation or music, etc.

Reduction of cortisol, CRF, stress axis.

Optimize sleep

8 hr sleep per night; melatonin 0.5mg po qhs; Trp 500mg po 3x/wk if awakening. Exclude sleep apnea.



30-60' per day, 4-6 days/wk


Brain stimulation

Posit or related


Homocysteine <7

Me-B12, MTHF, P5P; TMG if necessary


Serum B12 >500



CRP <1.0; A/G >1.5

Anti-inflammatory diet; curcumin; DHA/EPA; optimize hygiene

Critical role of inflammation in AD

Fasting insulin <7; HgbA1c <5.5

Diet as above

Type II diabetes-AD relationship

Hormone balance

Optimize fT3, fT4, E2, T, progesterone, pregnenolone, cortisol


GI health

Repair if needed; prebiotics and probiotics

Avoid inflammation, autoimmunity

Reduction of Aβ

Curcumin, Ashwagandha


Cognitive enhancement

Bacopa monniera, MgT


25OH-D3 = 50-100ng/ml

Vitamins D3, K2


Increase NGF

H. erinaceus or ALCAR


Provide synaptic structural components

Citicoline, DHA


Optimize antioxidants

Mixed tocopherols and tocotrienols, Se, blueberries, NAC, ascorbate, α-lipoic acid


Optimize Zn:fCu ratio

Depends on values obtained


Ensure nocturnal oxygenation

Exclude or treat sleep apnea


Optimize mitochondrial function

CoQ or ubiquinol, α-lipoic acid, PQQ, NAC, ALCAR, Se, Zn, resveratrol, ascorbate, thiamine


Increase focus

Pantothenic acid

Acetylcholine synthesis requirement

Increase SirT1 function



Exclude heavy metal toxicity

Evaluate Hg, Pb, Cd; chelate if indicated

CNS effects of heavy metals

MCT effects

Coconut oil or Axona


CHO, carbohydrates; Hg, mercury; Pb, lead; Cd, cadmium; MCT, medium chain triglycerides; PQQ, polyquinoline quinone; NAC, N-acetyl cysteine; CoQ, coenzyme Q; ALCAR, acetyl-L-carnitine; DHA, docosahexaenoic acid; MgT, magnesium threonate; fT3, free triiodothyronine; fT4, free thyroxine; E2, estradiol; T, testosterone; Me-B12, methylcobalamin; MTHF, methyltetrahydrofolate; P5P, pyridoxal-5-phosphate; TMG, trimethylglycine; Trp, tryptophan

Office News
We will be closed Monday Sept 7th for Labor Day.  Hope you have a fun 3 day weekend!