Choke faux 'choke

The recent winter storms have caused some early, juvenile green 'ulu fruit fall from the ma'afala ulu tree. Maryruth cooks and peels it to make a very artichoke-heart flavored side dish.

A new cover-up REVEALED!

Well, actually, it was an old cover-up, from the nineteen-sixties. Nevertheless, it was a cover-up! Conspiracy theory lovers, rejoice! The sugar industry seems to have covered up evidence sugar increases cancer risk. A news perspective HERE.



Sugar industry sponsorship of germ-free rodent studies linking sucrose to hyperlipidemia and cancer: An historical analysis of internal documents

Cristin E. Kearns, Dorie Apollonio, Stanton A. Glantz

PLOS Biology 15(11): e2003460

Published: November 21, 2017


In 1965, the Sugar Research Foundation (SRF) secretly funded a review in the New England Journal of Medicine that discounted evidence linking sucrose consumption to blood lipid levels and hence coronary heart disease (CHD). SRF subsequently funded animal research to evaluate sucrose’s CHD risks. The objective of this study was to examine the planning, funding, and internal evaluation of an SRF-funded research project titled “Project 259: Dietary Carbohydrate and Blood Lipids in Germ-Free Rats,” led by Dr. W.F.R. Pover at the University of Birmingham, Birmingham, United Kingdom, between 1967 and 1971. A narrative case study method was used to assess SRF Project 259 from 1967 to 1971 based on sugar industry internal documents. Project 259 found a statistically significant decrease in serum triglycerides in germ-free rats fed a high sugar diet compared to conventional rats fed a basic PRM diet (a pelleted diet containing cereal meals, soybean meals, whitefish meal, and dried yeast, fortified with a balanced vitamin supplement and trace element mixture). The results suggested to SRF that gut microbiota have a causal role in carbohydrate-induced hypertriglyceridemia. A study comparing conventional rats fed a high-sugar diet to those fed a high-starch diet suggested that sucrose consumption might be associated with elevated levels of beta-glucuronidase, an enzyme previously associated with bladder cancer in humans. SRF terminated Project 259 without publishing the results. The sugar industry did not disclose evidence of harm from animal studies that would have (1) strengthened the case that the CHD risk of sucrose is greater than starch and (2) caused sucrose to be scrutinized as a potential carcinogen. The influence of the gut microbiota in the differential effects of sucrose and starch on blood lipids, as well as the influence of carbohydrate quality on beta-glucuronidase and cancer activity, deserve further scrutiny.

Study reports a longterm effect of processing speed training on risk of dementia

The ACTIVE trial was a trail of three different training programs using computers on the risk of future Alzheimer dementia: memory training, reasoning training, and visual-motor response speed training. The training programs were done in persons over age 65, and the program s were completed within 3 years. The study had previously reported no change in risk of dementia by any of these interventions at 5 years, but follow up has continued, and the study now reports a significant improvement in the 10 year risk of dementia at 10 years.

Speed of processing is a skill which is used in team sports and in driving in the presence of other vehicles and pedestrians.

The dropout rate from the treatment phase did not have an impact on study results, but the number of visual-motor training sessions had a significant impact on dementia risk at 10 years but not 5 years.

Because the study is ongoing with multiple endpoints, and because the significant measure was not a planned primary outcome but a result of further analysis during follow up, it will need to be confirmed with a further trial to be accepted as fully valid for making future clinical recommendations. In the meantime perhaps the types of video games that require rapid response to unexpected changes in both center and periphery of a busy screen might be recommended to persons at risk for dementia.



Speed of processing training results in lower risk of dementia

In Press, Uncorrected Proof

Alzheimer's & Dementia: Translational Research & Clinical Interventions Authors: Jerri D.Edwards, Huiping Xu, Daniel O.Clark,Lin T.Guey,Lesley A.Ross,Frederick W.Unverzagt


• A randomized trial examined the efficacy of three cognitive training programs.

• Speed of processing cognitive training significantly reduced dementia risk.

• Each session of speed training completed was associated with reduced dementia risk.



Cognitive training improves cognitive performance and delays functional impairment, but its effects on dementia are not known. We examined whether three different types of cognitive training lowered the risk of dementia across 10 years of follow-up relative to control and if greater number of training sessions attended was associated with lower dementia risk.


The Advanced Cognitive Training in Vital Elderly (NCT00298558) study was a randomized controlled trial (N = 2802) among initially healthy older adults, which examined the efficacy of three cognitive training programs (memory, reasoning, or speed of processing) relative to a no-contact control condition. Up to 10 training sessions were delivered over 6 weeks with up to four sessions of booster training delivered at 11 months and a second set of up to four booster sessions at 35 months. Outcome assessments were taken immediately after intervention and at intervals over 10 years. Dementia was defined using a combination of interview- and performance-based methods.


A total of 260 cases of dementia were identified during the follow-up. Speed training resulted in reduced risk of dementia (hazard ratio [HR] 0.71, 95% confidence interval [CI] 0.50–0.998, P = .049) compared to control, but memory and reasoning training did not (HR 0.79, 95% CI 0.57–1.11, P = .177 and HR 0.79, 95% CI 0.56–1.10, P = .163, respectively). Each additional speed training session was associated with a 10% lower hazard for dementia (unadjusted HR, 0.90; 95% CI, 0.85–0.95, P < .001).


Initially, healthy older adults randomized to speed of processing cognitive training had a 29% reduction in their risk of dementia after 10 years of follow-up compared to the untreated control group.

Increased risk of dementia following herpes zoster ophthalmicus

The study below documents a 3-fold increased risk of dementia in elderly patients following herpes zoster (shingles) of the upper face, which often involves the eyelid and eye. Why should this be? The suspicion is that there would be either a vasculitis causing ischemic damage to the cerebrum or perhaps a subclinical encephalitis, or even both. Either of these otherwise silent complications of herpes zoster in the trigeminal distribution might lessen cerebral reserves, activating or accelerating an incipient dementia.

Should we be treating such zoster with larger and longer doses of antivirals? Could that help? Certainly there is much that is unknown about risk factor modification in incipient dementia.



Increased risk of dementia following herpes zoster ophthalmicus

Ming-Chieh Tsai, Wan-Ling Cheng, Jau-Jiuan Sheu, Chung-Chien Huang , Ben-Chang Shia , Li-Ting Kao , Herng-Ching Lin

Published: November 22, 2017


This retrospective cohort study aimed to examine the relationship between herpes zoster ophthalmicus (HZO) and the subsequent risk of dementia using a population-based database. We retrieved the study sample from the Taiwan Longitudinal Health Insurance Database 2005. The study group included 846 patients with HZO, and the comparison group included 2538 patients without HZO. Each patient was individually followed for a 5-year period to identify those patients who subsequently received a diagnosis of dementia. We performed a Cox proportional hazards regression to calculate the hazard ratios (HRs) along with 95% confidence intervals (CIs) for dementia during the follow-up period between patients with HZO and comparison patients. The respective incidence rates of dementia per 1000 person-years were 10.15 (95% CI: 7.22~13.87) and 3.61 (95% CI: 2.61~4.89) for patients with HZO and comparison patients. The Cox proportional analysis showed that the crude HR of dementia during the 5-year follow-up period was 2.83 (95% CI: 1.83–4.37) for patients with HZO than comparison patients. After adjusting for patients’ characteristics and comorbidities, HZO patients were still at a 2.97-fold greater risk than comparison patients for developing dementia. Furthermore, we found that of sampled male patients, the crude HR of dementia for patients with HZO was as high as 3.35 (95% CI = 1.79–6.28) compared to comparison patients. This study demonstrated an association between HZO and dementia. Clinicians must be alert to suspect dementia in patients with cognitive impairment who had prior HZO.

Multiple sclerosis and the Gut Microbiome: Some Preclinical Results

The gut microbiome is measured by assessing the prokaryotic DNA of a stool sample, which reflects the various types of bacteria that are generally commensal, beneficial residents of our gut in the normal human.

In the past 10 years it has become apparent that our gut microbiome can be quite different between individuals based on diet and region, and that persons with many different diseases can have characteristic differences in their gut microbiome from the average normal gut microbiome.

One hypothesis regarding these differences is that the gut microbiome in disease states is not reflecting the effect of disease, but instead may be one of its causes, especially as some type of enabling or modulating cause of a pertubation of immunity in autoimmune disease.

How do we tell cause from effect in such a case? One method is to see if a transfer of microbiome between healthy and diseased makes a difference.The study below reports results of such transfers (but to mice from human with MS).



in PNAS October 3, 2017 vol. 114 no. 40 10713-10718

Gut bacteria from multiple sclerosis patients modulate human T cells and exacerbate symptoms in mouse models Egle Cekanaviciutea,1,2, Bryan B. Yoob,1, Tessel F. Runiaa,3, Justine W. Debeliusc, Sneha Singha, Charlotte A. Nelsona, Rachel Kannera, Yadira Bencosmed, Yun Kyung Leeb,4, Stephen L. Hausera, Elizabeth Crabtree-Hartmana, Ilana Katz Sandd, Mar Gaciasd, Yungjiao Zhud, Patrizia Casacciad,e, Bruce A. C. Creea, Rob Knightc, Sarkis K. Mazmanianb, and Sergio E. Baranzinia,5

Edited by Lawrence Steinman, Stanford University School of Medicine, Stanford, CA, and approved August 7, 2017 (received for review June 30, 2017)


We have experimentally investigated the immunoregulatory effects of human gut microbiota in multiple sclerosis (MS). We have identified specific bacteria that are associated with MS and demonstrated that these bacteria regulate T lymphocyte-mediated adaptive immune responses and contribute to the proinflammatory environment in vitro and in vivo. Thus, our results expand the knowledge of the microbial regulation of immunity and may provide a basis for the development of microbiome-based therapeutics in autoimmune diseases.

The gut microbiota regulates T cell functions throughout the body. We hypothesized that intestinal bacteria impact the pathogenesis of multiple sclerosis (MS), an autoimmune disorder of the CNS and thus analyzed the microbiomes of 71 MS patients not undergoing treatment and 71 healthy controls. Although no major shifts in microbial community structure were found, we identified specific bacterial taxa that were significantly associated with MS. Akkermansia muciniphila and Acinetobacter calcoaceticus, both increased in MS patients, induced proinflammatory responses in human peripheral blood mononuclear cells and in monocolonized mice. In contrast, Parabacteroides distasonis, which was reduced in MS patients, stimulated antiinflammatory IL-10–expressing human CD4+CD25+ T cells and IL-10+FoxP3+ Tregs in mice. Finally, microbiota transplants from MS patients into germ-free mice resulted in more severe symptoms of experimental autoimmune encephalomyelitis and reduced proportions of IL-10+ Tregs compared with mice “humanized” with microbiota from healthy controls. This study identifies specific human gut bacteria that regulate adaptive autoimmune responses, suggesting therapeutic targeting of the microbiota as a treatment for MS.

On the ontology of "Absence makes the heart grow fonder."

"What would not I give to wander
Where my old companions dwell?
Absence makes the heart grow fonder;
Isle of Beauty, fare thee well!"

-- Thomas Haynes Bayly, 1844

What is this thing called an absence? Does an absence exist?

Absences, like holes, have an uncertain kind of existence, since some deny they actually exist, except as conformations of the stuff around them, of which they they are holes, or absences. But no one can deny that holes and absences can be measured and counted. From a scientific point of view, holes thus exist as much as any other objective phenomena that can be measured and counted can be said to exist.

And holes, of course, are emergent. They could not exist without the stuff of which they are NOT made.

Choke faux 'choke

The recent winter storms have caused some early, juvenile green 'ulu fruit fall from the ma'afala ulu tree. Maryruth cooks and pee...