The Best Chiropractic Care in Mesa, Arizona
by James Bogash
Relationship between Helicobacter pylori infection and Alzheimer disease
While I don’t think the relationship is causal, I thought I’d put this out there anyway. Long term readers of Updates will know that I view H. pylori infection as opportunistic rather than pathogenic.
Because of this, it is likely that those lifestyle factors that make an ideal environment for growth of H. pylori will also increase risk of AD.
by James Bogash
Docosahexaenoic acid: A positive modulator of Akt signaling in neuronal survival
While this may get a little too deep into biochemistry for most of us, the bottom line is that certain types of healthy fats are protective to our brain. This is yet another reason to believe that many of our neurodegenerative diseases such as Alzheimers and Parkinson’s are indeed diseases of lifestyle. Less intake of healthy fats over a lifetime leaves brain cells more susceptible to damage and cell death.
by James Bogash
High total cholesterol levels in late life associated w/ reduced risk of dementia
I just had a discussion with a patient today in which I showed concern with the increasingly aggressive approach mainstream medicine is taking with statin drugs. “Medicine for the masses” is a great thing for society, but for the individual patient it just plain sucks.
This study is perfect example of what may happen if we blanket everyone with the same approach. As to why cholesterol may be protective, I can’t explain at this time. But, what I do tell patients is to clean up their lifestyle and not worry so much about where their cholesterol is. If a patient has an otherwise good lifestyle but may have a cholesterol of 220 or 250, than I usually tell the patient not to worry.
The other beneficial compounds in their diet will protect the cholesterol from being damage and causing problems within our cardiovascular system.
by James Bogash
It may be generations before rising rates of Alzheimer’s dementia and Parkinson’s rates will stop increasing. One of my pet peeves in the average medical practice today is that we continue to remain decades behind research. It is this delay that will keep the next generation from avoiding Alzheimers dementia.
Why is this? Because it is very clear that the damage to the brain that occurs in Alzheimer’s and Parkinson’s begin decades before symptoms appear. For Parkinson’s, we know that, by the time symptoms are present, 70% of the brain cells in a specific region of the brain have died. 70%.
That means that, in anyone who has had a family history of these neurodegenerative conditions, there is a high likelihood that damage has already begun.
So, while patients I have come across who have this family history and are concerned about also developing the disease, none understand that the process has already begun.
Hopefully, this particular article will make this a little more clear. Basically, researchers looked at the hippocampal region of the brain (the area principally affected in Alzheimer’s) and found that this region had begun to atrophy (shrink).
Even more to the point, the brain had begun to shrink WITHOUT any cognitive loss. Clearly, the damage was already occurring, but it would yet be years before symptoms are evident.
If you have a family history of Alzheimer’s, or if you do not want to be the one to start the family history in your family tree, changes need to start now. These changes have been addressed in prior posts and can be viewed here.
In the meantime, if you have a family history of Alzheimer’s, have you been told that your brain may already been at risk?
by James Bogash
I’ll admit it. I’m no fan of drugs to lower cholesterol. 30+ blog posts on the topic should convict me. But linking statins to dementia is new news even to me.
To understand this association, there are two things you need to understand.
First, statins like Lipitor, Crestor and Zocor block an enzyme called HMG-CoA reductase. This is the enzyme that produces cholesterol in our bodies. However, this enzyme also produces a tiny little compound called Coenzyme Q10.
You may have heard of CoQ10 before because it is absolutely essential to make energy in every one of our cells. CoQ10 has been shown to play a role in various chronic diseases and conditions. They may include:
The other factor to understand for this post is that Alzheimer’s disease is associated with the presence of two abnormal proteins in the brain, called neurofibullary tangles (NFT) and amyloid plaques (AP) made up of tau proteins. It is pretty clear that these proteins are the result of damage to the brain, rather than creating the disease.
So, we can understand that anything that increases the production of tao protein is probably not a good thing.
By now, you can probably guess what prescription medication was shown to increase the production of tao protein in this particular study.
Yep.
The statin class of drugs was shown to increase the presence of tao protein. If you combine this fact with the well accepted fact that statins reduce blood levels of CoQ10 and CoQ10 plays a distinct role in Alzheimer’s disease progression, you can see a serious problem here.
The bottom line? Lowering your cholesterol with statins may make your cholesterol levels look better, but the list of problems this class of drugs contributes to get longer all the time. This leaves lifestyles changes as the only viable option.
If you are taking statins to lower your cholesterol, tell me some concerns you may have over the long term damage that may be occurring…
by James Bogash
Anyone who has seen the deterioration that occurs in Alzheimer’s dementia firsthand is fearful of the same thing happening to their own brain. Luckily, this is not an inevitable process.
To understand how cognitive loss and Alzheimer’s occurs, we need to understand more about my personal favorite part of the cell, the mitochondria.
The mitochondria is the portion of every cell in our bodies that helps to generate energy for the cell to function. Our brain cells, called neurons, require tremendous amounts of energy just to function at a basic level. When our neurons cannot generate the energy they need just to function at a basic level, they begin to break down and die off.
This means that anything that is good for our mitochondria will lower your risk of cognitive decline and Alzheimer’s, while anything that harms our mitochondria will increase the risk. It boils down to being this simple.
One thing that is very bad for our brain is being prediabetic or diabetic, and we have known for some time that these conditions increase the risk of Alzheimer’s. The relationship has been considered strong enough to call Alzheimer’s and Parkinson’s diseases “Type 3 Diabetes.”
This particular study adds weight to prior evidence and adds some specifics. Researchers looked at the risk that diabetes creates for loss of cognitive function. Findings include:
These are some scary numbers. So what can we do to protect our brain and lower our risk?
Obviously, an anti-diabetic lifestyle is key. Specifically, these changes can help greatly:
Overall, the progression to increasing loss of brain function (from mild cognitive impairment to terminal Alzheimer’s) is almost entirely under your control, but you need to start today. The damage to your brain begins decades before any symptoms are noticed. Every day you wait to make positive changes will lead to more brain cells lost.
What changes have you made to protect your brain?
by James Bogash
Antidepressant-like effects of cranial stimulation w/in low-energy magnetic field in rats
This study raises some very interesting questions and concerns. First, there is the therapy aspect–might some form of electrical/magnetic stimulation positively affect our mood? Next, what about deleterious effects of cell phones, microwaves, headphones, diagnostic testing, etc…?
I personally think that, when all the chips fall, in 30 yrs or so we will find that cell phone use has increased the risk/rate of some conditions like ADD/ADHD, brain tumors, seizures, Alzheimer/Parkinson’s.
by James Bogash
Zinc inhibition of gamma-aminobutyric acid transporter 4 (GAT4) reveals a link between excitatory and inhibitory neurotransmission
Sorry for the long title, but this one has some interesting implications. First, a bit on neurotransmitters. Glutamate is excitatory and stimulates the neuron to fire. Too much and you can ultimately burn out the neuron (this is one of the concerns with neuroexcitotoxins like MSG and aspartame).
GABA is inhibitory and counteracts the effects of glutamate. Many anti-seizure medications act by mimicking GABA. With this background, one of the long-time findings is that aluminum can increase risk of Alzheimer’s. Well, we know that aluminum knocks out zinc in the body, much like those perpetual motion ball thingies.
In this article, we see that synapses that release glutamate, which, in too high levels can damage a neuron, also release zinc at the same time to protect against overactive glutamate. It’s funny how we develop a theory or assumption, and years or even decades later we begin to elucidate exactly why the theory works.
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