New research has proposed a genetic explanation for the evolution of a bizarre method used by male butterflies to ensure the success of their sperm

The-Scientist.com, July 29, 2009, by Jef Akst  —  The sperm of male butterflies has a strange property. About 90% of it is non-fertile — essentially filler for the females’ sperm storage organs that tricks females into thinking they have all the sperm they need to fertilize their eggs. The males’ ploy reduces the likelihood that their mates will take another suitor, thereby ensuring their own paternity. A study published online today (July 29) in Biology Letters suggests that an intense battle of the sexes drove the evolution of non-fertile sperm.

“This study is an elegant and important advance in the understanding of this fascinating male:female co-evolution,” evolutionary biologist Matthew Gage of University of East Anglia in England, who was not involved in the research, wrote in an email to The Scientist.

Nonfertile sperm — or “kamikaze” sperm, as Gage calls them, because they “protect the male’s fertile sperm from competition” — are less costly to produce than fertile sperm. Previous work has suggested that males evolved them specifically to trigger the stretch receptors in the female sperm storage organs that allow them to monitor the amount of sperm in storage, Gage said. This is to the benefit of the male who deposited it, increasing the likelihood he will father a female’s offspring. But it’s to the detriment of the female, limiting the number of large, nutritious spermatophores she receives as gifts from her mates.

Such a conflict of interest between males and females of a species, an evolutionary predicament known as sexual conflict, often leads to genetic connections between the sexually antagonistic traits — in this case, between non-fertile sperm production and the number of mates a female takes. Such a connection might then facilitate the evolution of one or both of the traits. Previous work showed that males produced varying amounts of non-fertile sperm, and that females’ ability to store it varied as well, but until now, there was no evidence for a genetic tie between these two traits.

By comparing butterfly siblings from 25 different families as well as half siblings that shared a father, evolutionary biologist Nina Wedell of the University of Exeter in England and her colleagues found that males that produced more non-fertile sperm had sisters that mated less frequently. These results showed that the two traits are genetically correlated, “a hallmark of sexual conflict,” Wedell said in an email. Furthermore, “the existence of a genetic correlation between sperm production and storage means that, provided the benefit to one sex is larger than the cost in the other sex, the trait can rapidly be elaborated,” Wedell added. That may explain how non-fertile sperm came to compose such an enormous percentage of the ejaculate.

However, the interpretation of Wedell’s results requires some assumptions about the costs and benefits of non-fertile sperm production and storage that have not yet been confirmed, cautioned evolutionary biologist Darryl Gwynne of the University of Toronto, who was not involved in the work. The nutritious gifts that females receive upon mating is likely to be a high incentive for them to mate many times, but there are often costs associated with mating as well. It is therefore unclear how often females should mate to maximize their fitness.

“This paper addresses a really neat potential conflict situation in these butterflies,” Gwynne said, “[but you] need to show [that] by filling her sperm storage organs with these non-fertile sperm and increasing her refractory period, you’re actually impacting her fitness.” In other words, demonstrating that this is a case of sexual conflict requires showing that females incur a cost by storing non-fertile sperm.

In addition to identifying the fitness consequences for females, Wedell and her colleagues want to investigate the variation in male ejaculates. “These butterflies are born with all their sperm,” Wedell explained. “What we would like to know is, how do they decide how much sperm to deliver at each mating?”

“I spend 40 percent of my time away from my patients doing paperwork and getting prior authorizations,” said Jim King, MD, a family physician in Selmer, Tenn. “We need to start taking the barriers that are between me and my patients away.”


The U.S. has a catastrophically fragmented system that provides incentives for sick care instead of prevention. The system is in dire need of reform – reform to save lives, to save families and to save money for both patients and the American health care system.


It’s time to put our health back where it belongs, out of profit-motive insurance companies’ grasp and back into your and your doctor’s hands. It’s time to stand with more than 450,000 doctors who support health care reform.


When our friends at The American Academy of Family Physicians (AAFP) and Herndon Alliance (a nonpartisan coalition of more than 200 health-care provider organizations including the AARP, Mayo Clinic and Families USA) asked for our help, we produced this video featuring the doctors your family relies on for care. They are urging Americans to ‘Heal Health Care Now’.


Now, it’s your time to stand with more than 450,000 doctors who support health care reform. Make your voice heard and call Congress to reform health care: (202) 224-3121.


Thursday, July 30th at 12:15 PM ET Senate Majority Leader Harry Reid and Senators Durbin, Schumer and Murray will be having a press conference regarding what Doctors think about this issue.


The-Scientist.com, July 29, 2009, by Jef Akst  —  Researchers report a step forward in understanding the pathology of Alzheimer’s disease. Two genes that are commonly mutated in the early-onset form of Alzheimer’s may cause the disorder by altering how presynaptic neurons release neurotransmitters, according to a study published this week in Nature.

The mechanism may apply to other neurodegenerative disorders as well, the researchers say.

“This is a new concept that’s interesting to know,” said molecular neurobiologist Ilya Bezprozvanny of the Southwestern Medical Center at Dallas, who was not involved in the work.


More than 100 different mutations in two genes coding for the proteins presenilin 1 and 2 are associated with early-onset Alzheimer’s disease, but the exact effects of these mutations on neural function is still unclear. “It’s the first [study] suggesting that presenilins play a presynaptic role,” Bezprozvanny said.

In 2007, molecular geneticist and neuroscientist Jie Shen of Harvard Medical School and her colleagues created knockout mice that lacked both presenilin genes and found memory deficits and neurodegeneration in the brain — two key features of Alzheimer’s disease. In the current study, Shen set out to determine on which side of the synapse presenilins exert their effect by creating two strains of knockouts: one that lacked both presinilin genes only in the presynaptic neurons of a synapse in the hippocampus — a brain region that plays an important role in memory — and another where the genes were knocked out just post-synaptically.

Measuring neural activity in dissected brain sections from the two strains of knockout mice, the researchers were able to compare the effects of presenilins on pre- and post-synatpic activity. In presynaptic presenilin knockout mice, the researchers found drastically reduced long-term potentiation (LTP) — a physiological measure of memory formation. In postsynaptic presenilin knockouts, however, LTP was normal.

Knocking out presynaptic presenilins also altered other aspects of neuronal function and reduced the probability of neurotransmitter release. “Our earlier work led us to focus on NMDA receptors, which are postsynaptic receptors,” Shen said. “This [work] led us to see the importance of the presynaptic function.”

Neurotransmitter release depends on increases in calcium levels within the neuron. By blocking the release of calcium from the endoplasmic reticulum — an intracellular source of calcium — the researchers mimicked the effects of the presynaptic presenilin knockouts in control mice. This result points to intracellular calcium release as a possible mechanism by which presenilins regulate neuronal function.

“The main take home message is there is a difference in the way neurons process calcium levels in absence of presenilins, and that has an effect on synaptic [function],” said Bezprozvanny. However, he cautioned, it’s not clear how directly the findings can be applied to Alzheimer’s disease. “This is not an Alzheimer’s mouse model. This is a presenilin knockout.”

Researchers studying neurodegenerative diseases have long debated whether knocking out these genes is a good model for Alzheimer’s because the exact role of the many presenilin mutations associated with the disease is unclear. Some argue that these mutations result in a ‘loss of function,’ in which case a knockout model would appropriately represent the changes that occur in Alzheimer’s patients. Others argue that these mutations result in a ‘gain of function,’ or a change that cannot be replicated by knocking out the genes entirely.

If patients with Alzheimer’s disease do indeed have non-functioning presenilin genes, the results of this study may suggest that presynaptic neurotransmitter release is a more general mechanism of neurodegenerative diseases. For example, Shen and her colleagues found a presynaptic effect in a mouse model of Parkinson’s disease. These changes “might be a precursor to neurodegeneration,” Shen said, and might therefore provide new targets for disease therapies.

by Gabe Mirkin MD  —  If you need proof that exercise helps to keep you young, look at the exciting study from King’s College in London, England reported in the Archives of Internal Medicine (January 28, 2008). The researchers showed that people who exercise regularly have telomeres in the DNA of their white blood cells that are longer than those of couch potatoes. White blood cell telomeres shorten over time and serve as a marker of a person’s biological age.

The active ends of genetic material in cells are covered with a layer of proteins called telomeres. If they weren’t, the exposed ends of the genetic material would stick to anything nearby and the cells would die. However, each time a cell divides to make two cells, a little bit of the telomere is removed. Eventually the telomere is gone, the ends of genetic material stick together and the cell can no longer divide so it dies without replacing itself. Obviously, the longer the telomeres, the longer it will take for the telomeres to be used up so the cells are viable longer.

The study compared physical activity, smoking and socioeconomic status in 2,401 sets of twins. Those who were more active had longer leukocyte telomeres than those who were less active. The researchers concluded that “The mean difference in leukocyte telomere length between the most active (who performed an average of 199 minutes of physical activity per week) and the least active (16 minutes of physical activity per week) subjects was 200 nucleotides, which means that the most active subjects had telomeres the same length as sedentary individuals 10 years younger, on average.” – www.DrMirkin.com

DrMirkin.com, July 31, 2009, by Gabe Mirkin MD       In North America, more than 35 percent of the population

becomes diabetic, and most cases of diabetes could be prevented

with exercise.  A high rise in blood sugar levels causes sugar

to stick on the surface of cells. Once there, the sugar can never

get off and is eventually converted to sorbitol which destroys

the cell to causes all the side effects of diabetes such as

heart attacks, strokes, arteriosclerosis, nerve damage and so

forth (even in people who have not been diagnosed as diabetic).

So anything that prevents frequent high rises in blood sugar

helps to prevent cell damage.

       This month, a study showed that exercise lowered high

blood sugar levels in diabetics far more when done AFTER

eating dinner than before eating (Journal of the American Medical

Directors Association, July 2009).  Muscle contractions drive

sugar into cells with little or no insulin.  These people were

out-of-shape diabetics who walked slowly and for only 20 minutes.

Longer and more intense exercise lowers insulin and sugar levels

even more and would be even more beneficial.

       Another new study shows that you should exercise BEFORE

you eat because it lowers blood sugar levels the next morning

(Medicine and Science in Sports and Exercise, August 2009).

Nine healthy postmenopausal women exercised two hours on a

treadmill twice a day.  Those who exercised an hour before meals

had a much lower rise in blood sugar at 16 hours after eating,

compared to those who exercised an hour after their meals.

       Humans must use their muscles to stay healthy.

Contracting muscles before eating helps to prevent the rise in

blood sugar that follows meals, and exercising after eating helps

to keep blood sugar levels low the next morning.  Of course many

people do not have the time to exercise both before and after

meals, but you will benefit from exercising WHENEVER you can

because lowering blood sugar and blood fats helps to prolong

life and prevent diseases such as diabetes.  www.DrMirkin.com

Also Helps Cholesterol — But More Than A Sprinkle Required

WebMD.com, by Jeanie Lerche Davis  —  Several years ago a study showed that cinnamon can improve glucose and cholesterol levels in the blood. For people with type 2 diabetes, and those fighting high cholesterol, it’s important information.

Researchers have long speculated that foods, especially spices, could help treat diabetes. In lab studies, cinnamon, cloves, bay leaves, and turmeric have all shown promise in enhancing insulin’s action, writes researcher Alam Khan, PhD, with the NWFP Agricultural University in Peshawar, Pakistan. His study appears in the December issue of Diabetes Care.

Botanicals such as cinnamon can improve glucose metabolism and the overall condition of individuals with diabetes — improving cholesterol metabolism, removing artery-damaging free radicals from the blood, and improving function of small blood vessels, he explains. Onions, garlic, Korean ginseng, and flaxseed have the same effect.

In fact, studies with rabbits and rats show that fenugreek, curry, mustard seeds, and coriander have cholesterol-improving effects.

But this is the first study to actually pin down the effects of cinnamon, writes Kahn. Studies have shown that cinnamon extracts can increase glucose metabolism, triggering insulin release — which also affects cholesterol metabolism. Researchers speculated that cinnamon might improve both cholesterol and glucose. And it did!

The 60 men and women in Khan’s study had a diagnosis of type 2 diabetes for an average of 6 1-2 years but were not yet taking insulin. The participants in his study had been on antidiabetic drugs that cause an increase in the release of insulin. Each took either wheat-flour placebo capsules or 500 milligram cinnamon capsules.

  • Group 1 took 1 gram (two capsules equaling about one-quarter of a teaspoon) for 20 days.
  • Group 2 took 3 grams (six capsules, equaling a little less than one teaspoon) for 20 days.
  • Group 3 took 6 grams (12 capsules, equaling about one and three-quarters teaspoons) for 20 days.

Blood samples were taken at each level of the study.

Cinnamon made a difference! Twenty days after the cinnamon was stopped, there were significant reductions in blood glucose levels in all three groups that took cinnamon, ranging from 18 to 29%. But these was one peculiar finding that researchers don’t understand at this point. Only the group that consumed the lowest level of cinnamon continued with significantly improved glucose levels — group 1. The placebo groups didn’t get any significant differences.

Taking more cinnamon seems to improve the blood levels of fats called triglycerides. All the patients had better triglyceride levels in their 40-day tests — between 23% to 30% reductions. Those taking the most cinnamon had the best levels.

In groups taking cinnamon pills, blood cholesterol levels also went down, ranging from 13% to 26%; LDL cholesterol also known as “bad” cholesterol went down by 10% to 24% in only the 3- and 6-gram groups after 40 days. Effects on HDL (“good cholesterol”) were minor.

Cinnamon should be part of our daily diet — whether we have type 2 diabetes or not, writes Kahn. However, for the best effects, just a sprinkle isn’t enough.


                      and from www.consumerreports.org


Consuming about one-half teaspoon of cinnamon a day for 40 days reduced blood levels of both glucose and triglycerides, a potentially artery-clogging fat, by about 25 percent in adults with type 2 diabetes, a USDA clinical trial found. Cinnamon also cut “bad” LDL cholesterol by nearly 20 percent. And the benefits persisted for up to three weeks after people stopped taking it.