I am so excited! I finally pushed the button and published the first two books of my Toss Trilogy.
For the covers, I chose the pictures, and the incredible Ramona Lockwood designed the covers. You can see more of her work on her website.
If you’ve seen them, or read them, let me know what you liked…or didn’t.
Thanks. Until next time,
My Nebraska writing group just published a fantastic Christmas Anthology. The initial proceeds are be donated to a charity promoting literacy. Please check it out! Thanks.
This is the link to Love and Merry Christmas. Enjoy! And let me know how you liked my story!!
Four years ago, when Obama won the White House, I woke up disappointed my guy had lost, but with a good measure of hope. Maybe the president-elect would turn out to be a middle of the road guy. Maybe the responsibilities of office would wake him to the realities of the world.
It didn’t take long to find my hope was to be unfulfilled. In less than a year, a nation founded on freedom and individual responsibility began to transform into a welfare state. The solution to every problem was to throw money at it—money we didn’t have. In four years, our nation was owned by outsiders and we owed China more money than we were ever likely to be able to repay. Our leadership role in the world was abdicated in favor of fawning mediocrity. The permanent underclass had grown geometrically larger, and the future of American enterprise looked dim.
Today I woke to despair. My hopes for a recovery, a return to the principles upon which this nation was founded, are dead now. I can only cry for my country and for the grandchildren I love so much who will inherit a land crushed by debt, burdened by government intrusion into every aspect of life, and strangled by its disregard for individual life and liberty. First the defenseless young were destroyed, now the powerless elderly will be discarded.
So at nearly three in the morning, I sit in bed, unable to sleep. The sadness is overwhelming. I love this nation and never thought I would have to live to see it slide into defeat. T. S. Elliot was correct…
This is the way the world ends
This is the way the world ends
This is the way the world ends
Not with a bang but a whimper.
It’s time to look at the risk factors for Alzheimer’s disease. As most people know, there is no specific, single cause for Alzheimer’s. Rather, the disorder seems to be what scientist call multifactorial, which is just means there are many things that may contribute to it’s development.
Over the years, many possible causes have been researched.
For example, there are some specific gene mutations that are known to increase the likelihood of a person getting Alzheimer’s. Those gene mutations are most often found in well-studied groups of related people and result in familial Alzheimer’s disease, also called early onset Alzheimer’s disease. They account for roughly 10% of Alzheimer’s cases. Only one of these mutations, the one producing the epsilon 4 variety of a cholesterol-transport protein called Apoliporotein E, is likely to be found in the general population, where it could increase the likelihood of you or I having Alzheimer’s. Even then, it is only a risk factor, not an absolute cause, and is most dangerous only if you have inherited the epsilon 4 allele from both of your parents. (In other words, if instead of having one epsilon 4 allele, you have two—it can be argued that the double dose is enough to cause Alzheimer’s.) The frequency of the epsilon 4 allele in the general population runs from 12 to 14 percent in the sources I reviewed.
Other Risk Factors
Genes aside, what other risk factors can increase your chances of getting Alzheimer’s?
- Getting older. Though Alzheimer’s is NOT part of normal aging, it is more prevalent in older groups.
- Having a close blood relative (sibling or parent) with Alzheimer’s.
That’s the whole list for well-documented risk factors. Other factors which MAY (or may not) put you at higher risk for developing Alzheimer’s include
- Head trauma, especially multiple instances including loss of consciousness.
- A long history of high blood pressure.
- Being female (though this may simply be a reflection of the fact that women as a group live longer lives than men).
NOT Risk Factors
Some factors once considered possible causes of Alzheimer’s have been thoroughly studied and shown to NOT cause the disorder. These include
While the last two in particular are not good for brain cells, the damage they cause is not related to Alzheimer’s disease.
Nutritional deficiencies are not uncommon in persons with Alzheimer’s, but have never been shown to produce the disorder. In addition, supplements have never been shown to reliably improve the function of Alzheimer’s patients and cannot be shown to prevent the development of the disease.
Great care should be taken with supplements and herbal remedies. More is not necessarily better and it is possible to produce toxic effects if you take too much of almost any vitamin. (With the possible exception of vitamin C, since excess C is flushed from the body when we urinate.)
One herb in particular should be mentioned: Ginkgo biloba. Well-designed studies have shown that it does NOT lower your chance of developing dementia. And ginkgo can be dangerous if taken with blood thinners like Coumadin (warfarin) or with MAOIs (monoamine oxidase inhibitors—a group of antidepressants).
I would like to recommend two very good sources of information, written in understandable language. The first is a newsletter from Boston University. If you follow the link, it will take you to the newsletter. There is an excellent article called, “Reflecting on PAIRS,” that may be encouraging to those of you who are caregivers. The second is from Methodist hospital in Houston. I hope you find these helpful.
Apologies for running late this week. My husband came home yesterday after major surgery, and it’s been a less smooth transition than I’d hoped. But he is doing well now. Until next time…
We are critically examining the claims of the article, Astaxanthin: A Rising Star in Alzheimer’s Prevention. The last few articles in this series dealt with astaxanthin itself, but today we have reached the point where Dr. Mercola begins to talk about risk factors for Alzheimer’s disease.
The first thing he mentions is fructose.
Now, as a scientist, I take immediate offense at his impassioned diatribe against this simple sugar found naturally in fruits. HOWEVER, we are dealing once again with oversimplification leading to imprecision, and this time Dr. Mercola is the one oversimplifying.
It is entirely possible that if you read his articles regularly, you will already know what I am about to say. (I hope that is the case.) But the fructose controversy is alive and well in all types of media, so it is worth trying to shed a little light on what is really not so complex an issue.
1. What is fructose?
Fructose is a simple sugar found in fruits, berries, and some vegetables. It has the same chemical formula as glucose, the simple sugar preferred by brain neurons. That is, a molecule of either sugar contains six carbon atoms, six oxygen atoms and twelve hydrogen atoms.
The difference between fructose and glucose lies in the arrangement of the atoms. This is what they look like:
2. Does the difference in shape matter?
Well, yes, actually it does. If you read my earlier series of articles on drug discovery in Alzheimer’s, you may recall that 3-D shape is critical to protein function. Since it is the job of some proteins to make the energy from foods we eat available to our cells, it follows that the 3-D shape of the molecules in our food might also be important.
In the case of fructose and glucose, the difference in shape causes them to follow two different metabolic pathways. Glucose is dismantled very effectively by the metabolic machinery of cells and produces abundant energy in a form cells can easily use. Fructose is also metabolized, but it follows a different pathway than glucose does (because of its different shape) and becomes a free fatty acid instead of being converted easily to energy for the cell.
Your body can, and does, deal effectively with the fatty acids formed from fructose… up to a point. That point seems to be the amount of fatty acid formed from 25g of fructose per day. And therein lies the problem.
3. So what is the problem?
The problem is that many of us consume much more than 25g per day of fructose. And don’t blame the apple you ate at lunch. It is virtually impossible to exceed 25g per day of fructose if fresh fruits and vegetables are your only source. The culprit is the processed food we eat.
4. Have you heard of High Fructose Corn Syrup?
Of course you have! This highly concentrated natural sweetener is found in all kinds of processed food–not just cakes, pies and bread, but pizza dough, ketchup, mustard, soup, and more. It is almost impossible to find a food that hasn’t been sweetened by some company or other, these days. We have a natural, instinctive liking for sweet foods–and the food industry takes advantage of that by adding sweeteners to all sorts of things. Read the labels! Even things that should be healthy for you–dried fruit… simple, right?–may have been treated. I just read this on a container of trail mix: “dried sweetened cranberries.”
If you only ate 25g per day of fructose, but it came from high fructose corn syrup, would that be a problem? Probably not, though I know some would argue with me on that.
5. So foods sweetened with sugar are better for me, right?
I cannot bring myself to say that they are. Here’s the deal:
Table sugar, cane sugar, pure cane sugar… the chemical name for all of these is sucrose. Sucrose is a disaccharide. That is, it is made of two simple sugar molecules hooked together. (di- means two, -saccharide means sugar) Each molecule of sucrose is made from one molecule of glucose hooked to one molecule of fructose. If you look at the diagram above, you will see this. So what we call sugar is half glucose and half fructose, and most of us eat much more than we should of that combination. The sweetener in my trail mix was sugar. So how much sugar did it take to sweeten those dried cranberries? Well, the total sugars in 1/4 cup of trail mix was 7g. So if I eat a handful of trail mix four times in a day, and have NO OTHER SOURCE OF SUGAR IN MY DIET, I’m good. But what about the bread I made my lunch sandwich with? What about the cereal I ate for breakfast? What about the dressing on my dinner salad? You get the point.
Sugars are everywhere, they can contribute to obesity and to type 2 diabetes, and, in excess, will harm your body and your brain.
6. Isn’t fructose natural?
Of course it is. So is sugar. So is vitamin D. So is alcohol. Being natural does not mean something is good for you. There are no rules about what may be labeled natural. Natural is just a word the food industry uses to make you feel good about the processed foods you eat.
Why we love the word natural is beyond me. Spider venom is natural. Hurricanes and tsunamis and tornadoes are natural. All the poisonous plants in the world are natural. So when something is labeled “All Natural,” look a little closer at the label. Sometimes the product will actually be a healthy choice, other times not. You have to read the fine print.
7. Is there anything good to eat?
Yes. The best advice if you really want to eat healthy is to eat real food–fruits and vegetables you buy fresh (and organic, if you can afford it), meats that are hormone free. The most succinct advice I’ve seen on the subject was in a little book I browsed in my chiropractor’s waiting room. It said simply, “If your grandmother [or great-grandmother] wouldn’t recognize it as food, don’t eat it.” I have not forgotten the advice, though I don’t know who to thank for it. (If you know who the author was, please let me know so I can give proper credit!)
8. What about supplements?
I am not against them, with these caveats:
Remember that more is NOT always better (Too much of a good thing can be toxic.). Be sure to buy from a reputable vendor. Look carefully at the sources from which supplements are derived. Read the fine print.
I recommend reading this good, simple article on fructose and Alzheimer’s. It’s short and (dare I say it?) sweet. Enjoy.
Next time more on the presumed sources of Alzheimer’s disease.
See you then. –Susan
We’re talking about astaxanthin, the antioxidant touted in the online article, Astaxanthin: A Rising Star in Alzheimer’s Prevention, Among antioxidants, astaxanthin does appear to have some unique characteristics.
Tiny photosynthetic organisms found in marine environments—microalgae and phytoplankton, synthesize it. The richest natural source is the microalgae Haematococcus pluvialis. In addition, Roche pharmaceutical company began large-scale production of synthetic astaxanthin in 1990 (Ref. 3).
It appears that astaxanthin from H. pluvialis has high bioavailability, meaning it is well absorbed by the body. There is evidence (in rats) that it can protect living cells from damage by free radicals (Ref. 3). In vitro (in a test tube… literally in glass), astaxanthin has ten times higher antioxidant activity than other carotenoids, and 100 times higher antioxidant activity than vitamin E (Ref. 3).
Astaxanthin from H. pluvialis seems to be safe. A 2008 clinical study using astaxanthin to treat indigestion showed that 40 mg per day of H. pluvialis astaxanthin did not show any harmful effects during a 4-wk treatment period (Ref. 4). The original article cites a 2011 study that used 6 or 12 mg of astaxanthin for 12 weeks. I did not find any studies looking at longer than a 12-week period.
In the 12-week study, the researchers concluded that “concentrations of erythrocyte and plasma astaxanthin were not different between the 6 and 12 mg astaxanthin groups, suggesting that 6 mg astaxanthin is effective enough to show antioxidative benefit in vivo.” Those researchers were looking at decreases in markers for oxidative damage (the PLOOH mentioned in the original article) found in red blood cells and blood plasma (Ref. 7).
The same researchers have undertaken a new study testing daily doses from 3 to 6 mg of astaxanthin. Their concern is to find the lowest effective dosage. Finding the lowest effective dose is important, because when dealing with bioactive molecules, more is NOT necessarily better.
Numerous studies have shown that astaxanthin protects neuronal cells in rats and mice from oxidative damage. When researchers took neuron-like cells from a human cell line (human cells, often derived originally from cancers or tumors, that have been raised artificially for many years and many generations in laboratories) and exposed them to oxidative damage that would normally cause cell death, astaxanthin treatment was able to reduce the number of cells that died. (Refs. 5 and 6) The cells in this study were dopaminergic, which means that they use the neurotransmitter dopamine, similar to the cells that die in Parkinson’s disease.
Does that mean astaxanthin could help stop cell death in Parkinson’s? Maybe, but only if those cells are dying for the same reason as the cells in the study. You see, all we can ever do, prior to clinical testing results, is make an educated guess about what a supplement will or won’t do in humans.
And so far, clinical antioxidant studies looking for memory effects have not been too promising. They have found that vitamin E does not significantly slow down memory decline for Alzheimer’s patients or early Parkinson’s patients. Furthermore, a combination of vitamins E and C did not significantly improve college students’ performance on specific cognitive tasks. I was unable to access the “small clinical trial” that found astaxanthin “improved cognition.” I hope to remedy that problem before my next post.
Astaxanthin looks like a good antioxidant. It has extremely high antioxidant activity. It looks like it is probably safe. And it appears that the best source is H. pluvialis.
Would I spend a lot of money on one specific antioxidant supplement? No, not a lot of money. But if it was reasonably priced I might add one to my diet. Still, I always prefer real food to pills! And with real food, I know my body has been designed to do a good job of absorbing the nutrients (and antioxidants) I ingest.
The next section of the article goes into other avenues, some of which have been clearly shown to enhance brain health. More on that next time.
1) Eric A. Johnson and Gil-Hwan An, Astaxanthin from Microbial Sources, Critical Reviews in Biotechnology, 1991, Vol. 11, No. 4, pages 297-326.
2) Paola Palozza and Norman I. Krinsky, Astaxanthin and canthaxanthin are potent antioxidants in a membrane model, Archives of Biochemistry and Biophysics, 1992, Vol. 297, Issue 2, pages 291-295.
3) Jian-Ping Yuan, Juan Peng, Kai Yin and Jiang-Hai Wang, Potential health-promoting effects of astaxanthin: A high-value carotenoid mostly from microalgae, Mol. Nutr. Food Res.,2011, Vol. 55, pages150–165.
4) Kupcinskas, L., Lafolie, P., Lignell, A, Kiudelis, G. et al., Efficacy of the natural antioxidant astaxanthin in the treatment of functional dyspepsia in patients with or without Helicobacter pylori infection: a prospective, randomized, double blind, and placebo-controlled study, Phytomedicine,2008, Vol. 15, pages 391–399.
5) Ikeda, Y., Tsuji, S., Satoh, A., Ishikura, M. et al., Protective effects of astaxanthin on 6-hydroxydopamine-induced apoptosis in human neuroblastoma SH-SY5Y cells, J. Neurochem., 2008, Vol. 107,pages 1730–1740.
6) Liu, X. B., Shibata, T., Hisaka, S., Osawa, T., Astaxanthin inhibits reactive oxygen species-mediated cellular toxicity in dopaminergic SH-SY5Y cells via mitochondria-targeted protective mechanism, Brain Research, 2009, Vol. 1254,pages 18–27.
7) Kiyotaka Nakagawa, Takehiro Kiko, Taiki Miyazawa, Gregor Carpentero Burdeos, Fumiko Kimura, Akira Satoh and Teruo Miyazawa, Antioxidant effect of astaxanthin on phospholipid peroxidation in human erythrocytes, British Journal of Nutrition, 2011, Vol. 105, pages 1563–1571.