AF and dementia risk in patients younger than 67

Just more confirmation data from what we have learned over the last few years. I am not sure why some doctors still cling to the idea that more data needs to be gathered to prove that AF results in blood clots that increase dementia risk.

[www.the-hospitalist.org]

cited article link below
[archneur.jamanetwork.com]

I agree, Researcher.

We’ve long known that when hyperviscosity is present and with longer duration Afib, the risk of stroke increases. But, as is often so typical, medical research focus fails to investigate or emphasize the origins of health problems such as the multiple contributing factors that promote hyperviscosity; and just blame the Afib instead.

Here on this forum, we’ve discussed for years, the sticky, thick blood factor caused by environment, diet, lifestyle factors and genetic mutations. Those factors are typically prevalent in dementia as well.

Our well-examined magnesium deficiency topic is also linked to Alzheimer’s disease and we know low magnesium not only can promote Afib but also increased platelet aggregation.

Etiology is of critical importance for prevention and not just with dementia and Alzheimer’s.

Jackie


Blood Viscosity: The Role of Blood Flow in Cognitive Function
Monday, 18 June 2012
by Ralph E. Holsworth, DO, and Jonathan V. Wright, MD - Vol. 13, No. 2. Summer, 2012

In April 2012, the World Health Organization published a new report on the alarming worldwide trends in dementia. The report estimated that in 2010, approximately 35.6 million people were living with dementia. By 2030 that number is set to double to 65.7 million.

Blood viscosity has been demonstrated in multiple large clinical trials to have significant links with age-related cognitive impairment. The studies have established empirically the relationship between blood viscosity and cerebral blood flow—a relationship that is also highly intuitive. Importantly, blood viscosity is easily modifiable via nutritional, botanical and pharmacologic treatments.

The pattern of exponential increases in blood viscosity after the age of 60, as reported by the research group at the National Institute of Aging, helps to define an at-risk population that may benefit from blood viscosity monitoring and treatment. The availability of clinically practical instrumentation for blood viscosity measurement, such as is now available at Meridian Valley Laboratory, creates a new avenue for detecting and controlling age-related blood flow disturbances in mid-life and senior adults, especially those 60 years of age and greater.
Continue: [www.holisticprimarycare.net]


Altered Ionized Magnesium Levels in Mild-To-Moderate Alzheimer's Disease
Magnes Res. 2011; 24(3):115-21.
Barbagallo M, et al.

Summary
Magnesium deficiency is found in several chronic, age-related diseases: cardiovascular, metabolic and neuro-degenerative diseases. Alzheimer's disease (AD) is the most common cause of dementia. This research studied magnesium homeostasis in patients with mild to moderate AD. One hundred and one elderly (?65?years) patients were consecutively recruited (mean age: 73.4±0.8?years; M/F: 42/59). In all patients, a comprehensive geriatric assessment was performed including cognitive and functional status. Admission criteria for the AD group (diagnosed according to the DSM-IV and the NINCDS-ADRDA criteria) included: mild to moderate cognitive impairment (MMSE score: 11-24/30, corrected for age and education). Blood samples were analyzed for serum total magnesium (Mg-tot) and serum ionized magnesium (Mg-ion). AD patients had significantly lower MMSE scores, and for the physical function tests. Mg-ion was significantly lower in the AD group as compared to age-matched control adults without AD. No significant differences were found in Mg-tot between the two groups. For all subjects, Mg-ion levels were significantly and directly related only to cognitive function, while no significant correlations were found in this group of patients between magnesium and ADL or IADL. Our results show the presence of subclinical alterations in Mg-ion in patients with mild to moderate AD.
[www.ncbi.nlm.nih.gov]

Lifestyle:
Eur J Intern Med. 2011 Apr;22(2):134-40. doi: 10.1016/j.ejim.2010.12.017. Epub 2011 Jan 26.
Nutrition and Alzheimer's disease: the detrimental role of a high carbohydrate diet.
Seneff S1, Wainwright G, Mascitelli L.

Abstract
Alzheimer's disease is a devastating disease whose recent increase in incidence rates has broad implications for rising health care costs. Huge amounts of research money are currently being invested in seeking the underlying cause, with corresponding progress in understanding the disease progression. In this paper, we highlight how an excess of dietary carbohydrates, particularly fructose, alongside a relative deficiency in dietary fats and cholesterol, may lead to the development of Alzheimer's disease. A first step in the pathophysiology of the disease is represented by advanced glycation end-products in crucial plasma proteins concerned with fat, cholesterol, and oxygen transport. This leads to cholesterol deficiency in neurons, which significantly impairs their ability to function. Over time, a cascade response leads to impaired glutamate signaling, increased oxidative damage, mitochondrial and lysosomal dysfunction, increased risk to microbial infection, and, ultimately, apoptosis. Other neurodegenerative diseases share many properties with Alzheimer's disease, and may also be due in large part to this same underlying cause.
Copyright © 2011 European Federation of Internal Medicine. PMID: 21402242 [PubMed - indexed for MEDLINE]


Cardiovascular 03.04.2013
Atrial fibrillation carries a significant risk for cognitive decline, even when stroke is not involved, a meta-analysis found.
In 14 observational and prospective studies of patients with or without stroke, the relative risk of cognitive impairment was 1.40 (95% CI 1.19 to 1.64), according to Jeremy N. Ruskin, MD, of Massachusetts General Hospital, and colleagues.

The risk was similar when researchers excluded cognitive impairment and analyzed the studies only for dementia, “which is more reliably diagnosed than cognitive impairment,” (RR 1.38, 95% CI 1.22 to 1.56), they reported March 4 (2013) in the Annals of Internal Medicine. [www.medpagetoday.com]

Alzheimer’s disease is the fastest growing health threat in the United States according to a new landmark report from researchers at the University of Washington, Seattle. A 2013 study in the journal Neurology found that the number of people with Alzheimer’s disease will jump from 4.7 million to 13.8 million by 2050. Associated health care costs will skyrocket from $200 billion to more than $1 trillion by 2050, increasing the cost of Medicaid and Medicare by 500 percent.

In America, a new case of Alzheimer’s develops every 68 seconds; by 2050, the incidence will increase to every 33 seconds.

Hi researcher and Jackie,

Yes this retrospective population study out of Rotterdam simply adds more confirmation to this key issue of the ever stronger association between AFIB and Dementia/Alzheimer's as a key driver and inspiration for NOT just settling for 'living with the beast'. We have reported now multiple times over the last few years in the AFIB report on this now front and center major concern for AFIB patients long term.

The Utah group of Drs Day, Jared Bunch and Peter Weiss etc, have been leaders too for the last half decade in exploring this relationship and were the first to my knowledge to draw the clear link between early onset Dementia in younger AFIB patients being a real smoking gun.

The solution is not just park people on OAC drugs either, as the same Utah group has underscored that too much time out of anticoagulation range ( mostly tested with Warfarin patients obviously) is a key associated like with many of these early onset Dementia cases. More recently, increasing evidence points to the possibility that long term full strength OAC therapy might contribute to microbleeds overtime that 'might' be a key driver of this dementia onset.

This all jsut reinforces our core protocol and philosophy which is to promote cessation of AFIB by whatever combined means possible and beign open to using ALL the best tools at our behest and not become too dogmatically attached to one approach at the exclusion of other sound methods.

All these years when Cardios and EPs told patients that as long as you get your rate under 100bpm and stay on OAC AFIB is no big deal, they simply never made the connection, nor investigated how many of their long-time afibbers who they eventually lost track of and never heard from again, had developed Dementia or Alzheimers and likely fell off the AFIB doctor visit routine.

As such, it took a long time for the gradual weight of the evidence to increase to the point where so many Cardios and EPs did finally start to notice these increased numbers of patients suffering from AFIB and cognitive decline. This, then, became the inspiration for these many large ongoing studies now that have universally all confirmed this association so far when the issue has been investigated.

I would not be surprised, if when this connection is more fully fleshed-out in the coming years, that we discover the Dementia issue is even a far bigger issue, statistically speaking, than is the frank stroke risk for afibbers. Meaning that the total burden of AFIB manifesting across the full spectrum of silent cerebral ischemic changes, including microemboli and microbleeds, as well as TIA to full-blown strokes should be a good deal larger than the actual stroke events alone.

All the more reason to do everything in our power naturally and in conjunction with your EPs help as well to end the cycle of AFIB in each of our lives to the greatest extent possible and the sooner the better.

Continuing to procrastinate for years based on merely slowing down AFIB to some degree but with still a fair amount of increasing episodes each year, is not a winning bargain long term. Again, if our life-style risk factor management efforts in combination with dedicated CVD/OSA/Metabolic Syndrome/ Obesity control efforts prove anything less than near totally effective in suppressing one's AFIB events after a full year of such effort, then by all means seek out the most experienced AFIB ablation operator available to you to add that often key step in the whole process without further delay.

Shannon

There is a book "let food be your medicine" by Don Colbert M.D. of Orlando, Florida, he is a Holistic doctor. Dr. Colbert says that dementia is Type III diabetes, he says that the cells of the body become resistant to Insulin which causes diabetes. Dr. Colbert says that the cells of the brain don't open up to take in insulin, the cells will then start to die, just like in diabetes, he says that top scientists in the world are saying this. Dementia is becoming the 6th leading cause of death, sugar and processed starches are contributing to these diseases, says to eat low glycemic starches, I have ordered this book, it is just brand new on the market.

Liz

I’m very glad to see there is now a book on this topic, Elizabeth. I look forward to your summary post after you've read it.

Type 3 Diabetes and the brain connection have been discussed by many of the well known functional medicine type practitioners for at least 10 years if not longer. Dr. Rosedale and Dr. Blaylock have discussed as has Dr. Mercola with several early reports indicating the connection. Not many people have been listening or seem interested, yet, tragically, the increased brain involvement continues to escalate and the high carb diets remain the norm for a huge percentage of people… (witness also the increasing obesity epidemic) although not all dementia/Alzheimer victims are obese. My two friends were thin.

So, I’m delighted to learn there is a book we can recommend to those who want to take this dementia threat seriously while there is still time to prevent the almost guaranteed brain involvement.

Thanks for the news!

Jackie



Clip from Dr. Mercola’s column:

New Kid on the Block: Type 3 Diabetes, or 'Brain Diabetes,' May Be Responsible for Alzheimer's Disease and Glaucoma
A growing body of research suggests there's a powerful connection between your diet and your risk of both Alzheimer's disease and glaucoma,10 via similar pathways that cause type 2 diabetes. Alzheimer's disease was tentatively dubbed "type 3 diabetes" in early 2005 when researchers learned that the pancreas is not the only organ that produces insulin. Your brain also produces insulin, and this brain insulin is necessary for the survival of your brain cells.

A drop in insulin production in your brain may contribute to the degeneration of your brain cells, and studies have found that people with lower levels of insulin and insulin receptors in their brain often have Alzheimer's disease. Researchers have now discovered that insulin does far more than simply regulating blood sugar. Your brain does not require glucose, and actually functions better burning alternative fuels, especially ketones. In fact, Dr. Rosedale believes that it is the constant burning by the brain of glucose that is primarily to blame for Alzheimer's and other brain disorders.

Insulin is actually a "master multitasker" that helps with neuron glucose-uptake, and the regulation of neurotransmitters, like acetylcholine, which are crucial for memory and learning. This is why reducing the level of insulin in your brain impairs your cognition. Other research11 shows that type 2 diabetics lose more brain volume with age than expected—particularly gray matter. This kind of brain atrophy is yet another contributing factor for dementia. "Brain diabetes" may also be responsible for glaucoma, according to recent research. [articles.mercola.com]
Over 4,000 results for reports on Type 3 diabetes: [search.mercola.com]

Hey guys,

What level of afib burden are we talking about here? For example, i have had 5 episodes this year, ranging from 4-10 hours each. I'm 37 years old. Is this enough burden to worry about dementia in the long run?

I assume the answer is 'We don't know yet", but I wish it was clearer what kind of burden we are talking about.

Thanks!