Several months ago, pharmacist David had his two week vacation to southern states. Beaches, historical towns, and he even toured some prospectus colleges for his son in junior high. Everything went well except he got a little blood in his urine and semen. It’s not much. He got the similar situation a couple of years ago. And it went away after taking some 500 mg Ciprofloxacin bid for 10 days. Not this time though. Ciprofloxacin didn’t do a thing. His PCP introduced him to the urologist. He underwent many tests from finger exam, PSA test, cystoscopy, and all the way even to MRI, nothing adverse was found. He did his own web research. And the only thing made him relieved a bit was the data shown that, just a few percent of those become tumorous. And the majority of people have to live with it, no matter how mind bothering daily! David is a very good pharmacist for problem solving. He just doesn’t give up. “If nothing is found, and the bleeding is not end, should I try vitamin K instead”? He ordered the Natural K100 mcg. Miraculously, within a couple of days, the bleeding stopped! After a week, he cut the dose from 1 tab daily to half. Since then, his life has returned to perfect normal!
The FDA’s advisory board is considering to approve the Biogen’s Aducanumab for Alzheimer’s therapy, again, after years “reorganizing” the clinical data.
One says the possible mechanism is to help open the canal for garbage plaque to leave the brain, different from the other explanation such as of Eli Lily’s.
According to the prediction of Free Energy and Memory Protein Stability theory, just let the plaque proteins leave the brain, one can’t stop the memory protein loss. Thus Aducanumab will not stop the deterioration of early and middle stage Alzheimer’s disease.
What are the differences between IBS (irritable bowel syndrome) and IBD (inflammatory bowel disease)?
Not just because researches showed AD is caused by deprivation of glucose in brain (such as 1-31-2017 Temple Univ.), clinically many AD patients also show symptoms of overnight low glucose in brain: typically, nightmares, night sweats, and hallucinations. Especially during middle stage Alzheimer’s while some patients exhibit higher frequency of symptoms (about twice weekly). That period usually does not last very long ranging from a couple of months up to a year. Passing that critical period, those Alzheimer’s patients could advance to severe stage of AD, when patients typically lose their dignity and independence as described in Johns Hopkins Medicine (www.hopkinsmedicine.org). The underlying cause is explained as recurrent severe deprivation of glucose in brain breaks down memory structures and diminish enzyme activities, which in return triggers hormonal rescue mechanism to stimulate liver to generate sudden over flow of glucose into brain. These lack of glucose then causing spike of glucose roller coaster may eventually “kills” the brain, and make higher glucose content in the end stage of AD.
Thus a smooth supply of glucose during late night sleep is very critical if you or your loved ones experience those symptoms, since important REM sleep cycles requires higher level energy supply in brain to support memory function during this period!
Many recent years clinical and research results show deprivation of glucose in brain causing early stage Alzheimer’s disease, such as the study published on 1-31-2017 by the researchers in the medical school of Temple University. However, some study results may cause confusions without expertise analysis. For example, Yang and colleagues published an article “Evidence for brain glucose dysregulation in Alzheimer’s disease (Alzheimer’s & Dementia 14, 2018). This study correlated higher glucose level and diminished activity of glycolysis enzyme found in deceased AD patients. It ignored the clinical symptoms of nightmares, night sweats, and hallucinations that exist in most early stage AD patients. Those symptoms are typical of nocturnal hypoglycemia trigged rebound through hormonal rescue mechanism. It also ignored their own data that showed fasting glucose level correlation and failed to relate typical causing facts of Somogyi effect. Their conclusion should have emphasized the importance of early intervention of AD patients with timed supply of glucose at bedtime, instead of puzzling suggestion of higher glucose level causing the disease.
Thus, clinicians and caregivers should concentrate on their own knowledge on symptoms of AD patients, otherwise it can be misled by some studies.
Some people think that glucose, which is a form of sugar, must make people fat. As a matter of fact, the exact opposite can be true: it can suppress appetite. And according to this* study in the Proceedings of National Academy of Sciences, it is actually the “evil” twin brother fructose responsible for enticing never satisfied food desire.
The underlying reason is quite simple: the brain normally depends on glucose as its only source of energy. When we ingest fructose, it does not satisfy our brain’s energy needs, and our brain will keep prompting us to eat more.
Sucrose, or table sugar, is composed equally of fructose and glucose. So only half of the sugar most commonly added to food contributes to the brain’s energy needs. It also takes enzymes, time, and energy to break down sucrose into its constituent parts. So, sucrose, like fructose, is not nearly as appetite suppressing as ingesting glucose.
In contrast, the glucose in ChewFull readily diffuses into blood and circulates to the brain without requiring digestion, enzymes and energy to break it down into a usable energy source by the brain. By providing glucose to the brain before and during a meal, ChewFull immediately goes to work, sating our appetite by creating a feeling of fullness sooner than if we eat other sugars or only normal foods alone.
* PNAS, May 19, 2015, Vol.112, no.29, 6509-6514