A range of different high blood-pressure conditions of pregnancy predicted onset of cardiovascular events, chronic kidney disease, and diabetes over the subsequent decades, to varying degrees, over an average of about 40 years in the Northern Finland Birth Cohort 1966. In particular, new-onset gestational hypertension in about 10% of the cohort of greater than 10,000 women was associated with triple the risk of later fatal myocardial infarction, almost twice the risk of chronic kidney disease, and 45% to 60% increased risks of ischemic heart disease, ischemic stroke, and diabetes compared with women who remained normotensive during pregnancy.
Those adjusted risks were still significantly increased in an analysis that excluded women with traditional cardiovascular risk factors. Heart failure was significantly more likely over the follow-up among women who during pregnancy had isolated systolic hypertension, gestational hypertension, chronic hypertension, or preeclampsia or eclampsia. Diabetes was also predicted by isolated systolic hypertension and chronic hypertension.
Many reproductive-aged women already have cardiovascular risk factors, and pregnancy as a stressor may reveal their vulnerability as new-onset or worsening hypertension occurs during pregnancy. This suggests that poor metabolic health, not hypertension, leads to increased chronic disease risk. But even in the analysis of women without such cardiovascular risk factors as smoking, obesity, or advanced age, many of the risks remained significantly higher in those with many of the high-blood-pressure conditions, suggesting that hypertension during pregnancy has an independent effect on long-term risk.
In an editorial accompanying the group’s analysis, both of which were published in the February 12, 2013 issue of Circulation, Drs Suttira Intapad and Barbara T Alexander, University of Mississippi Medical Center, Jackson are especially impressed by the finding that nearly all of the studied high-blood-pressure conditions of pregnancy predicted postpartum onset of arterial hypertension, even in the absence of prepregnancy risk factors such as obesity and smoking.
The guidelines include preeclampsia as a risk factor for heart disease and stroke. Based on the current study, the assessment of cardiovascular risk in women should be expanded to include all classifications of hypertension during pregnancy and not just those diagnosed clinically as preeclampsia.
In a study to be presented on February 14 between 1:15 p.m., and 3:30 p.m. PST, at the Society for Maternal-Fetal Medicine’s annual meeting, The Pregnancy Meeting ™, in San Francisco, California, researchers will present data showing the effectiveness of preemptive treatment for hyperemesis gravidarum and severe morning sickness.
Hyperemesis gravidarum is a severe form of morning sickness which affects two percent of pregnant women. Hyperemesis gravidarum is marked by persistent nausea and vomiting, and can begin early in the first trimester, continuing well into the second, third or even up to giving birth. Women who suffer from hyperemesis gravidarum become severely dehydrated, and often end up in the hospital on intravenous fluids. Recurrence rate for women who had hyperemesis gravidarum in their first pregnancy is 75-85 percent in subsequent pregnancies, and the condition can be fatal. Previous treatment for hyperemesis gravidarum was to administer medication Diclectin in Canada, Bendectin in the US at the onset of symptoms, but this course of treatment provided little, if any, relief.
Drs. Gideon Koren and Caroline Maltepe, of The Hospital for Sick Children in Toronto, ON, Canada, divided 59 women with a history of hyperemesis gravidarum or severe morning sickness into two groups: one would begin taking Diclectin as soon as the pregnancy was discovered; the second group would begin treatment at the first sign of nausea. They found the group receiving treatment before the onset of symptoms, had a significant decrease in risk of severe nausea and vomiting. This is the first time there is an answer. Women who have experienced hyperemesis are so traumatized by it, they are afraid of a second pregnancy. Dr. Koren, who with Dr. Maltepe runs a severe morning sickness counseling program at The Hospital for Sick Children, says the drug used to treat hyperemesis gravidarum is safe to take throughout pregnancy or even before conception.
A copy of the abstract is available at http://www.smfmnewsroom.org
The Society for Maternal-Fetal Medicine established in 1977, is a non-profit membership group for obstetricians-gynecologists who have additional formal education and training in maternal-fetal medicine. The society is devoted to reducing high-risk pregnancy complications by providing continuing education to its 2,000 members on the latest pregnancy assessment and treatment methods. It also serves as an advocate for improving public policy, and expanding research funding and opportunities for maternal-fetal medicine. The group hosts an annual scientific meeting in which new ideas and research in the area of maternal-fetal medicine are unveiled and discussed. For more information, visit http://www.smfm.org or http://www.facebook.com/SocietyforMaternalFetalMedicine.
Heavenly View From The Alps
A New York-based physician-researcher from Touro College of Osteopathic Medicine, best known for his research into fertility and twinning, has uncovered a potential connection between autism and a specific growth protein that could eventually be used as a way to predict an infant’s propensity to later develop the disease. The protein, called insulin-like growth factor, is especially involved in the normal growth and development of babies’ brain cells. Based on findings of prior published studies, Touro researcher Gary Steinman, MD, PhD, suggests that depressed levels of insulin-like growth factor in the blood of newborns could potentially serve as a biomarker for the later development of autism. However, this connection has never been directly studied. Steinman presents his exciting theory in the journal Medical Hypotheses.
Insulin-like growth factor stimulates special cells in the brain to provide an essential insulating material, called myelin, around the developing nerves that is needed to efficiently transmit important messages about everything the brain controls, from physical functions such as movement to mental functions such as sensory perception, thinking and emotions. In the developing fetal and pediatric brain, myelin is also important for nerve fibers in one area of the brain to form proper pathways to other regions, allowing the body to hone functions over time. Insufficient insulin-like growth factor results in insufficient insulating material, as has been seen in brain biopsies of autistic individuals, and may impede proper pathway development. Steinman suggests that this potential relationship between neonatal insulin-like growth factor levels and autism be directly studied.
In the United States, autism is currently reported in 1 in 88 live births, about 125 new cases every day, and it is four times more common in boys than in girls. Women who have given birth to an autistic child have approximately a one-in-five chance of having another. The impact that this life-long disease has on children, families, and finances is enormous. An affected child could add as much as $3 million in lifetime medical expenses over an unaffected child.
Autism is on the rise, especially in the last two decades; either because of environmental factors, expanded diagnostic criteria, or both. Yet almost nothing is currently known about the predisposing molecular and histological changes that differentiate a newborn destined to be neurologically normal from an autistic one. Because no effective treatment or prevention for autism exists, research examining Steinman’s idea is critical, as it holds key to understanding the cause of this often devastating illness. Steinman recommends a study to look into this hypothesis, and if this study supports his theory that identification of reduced insulin-like growth factor at birth is later followed by the appearance of autistic characteristics, then the subsequent development of a simple biomarker blood test is just as decisive.
In the suggested study, a sample of umbilical cord blood would be collected immediately after birth to measure insulin-like growth factor. Alternatively, a routine heel-stick blood sample might be used, as these are already collected from newborns within a day or two after birth to test for inborn errors of metabolism in most U.S. hospitals. Then the data collected at birth is compared with the neurologic evaluation of the baby at 18 to 36 months of age. If successful, the next stage of suggested research involves detecting depressed insulin-like growth factor levels in amniotic fluid during the second trimester of pregnancy followed by supplementation of the growth factor before symptoms of autism develop.
“Further investigation into whether pharmaceutical treatment in the early postnatal period of newborns with a suspicion of a tendency of developing autism could reverse the effects of having had pathologically low levels of insulin-like growth factor while in utero and reduced insulin-like growth factor in their umbilical cord blood at birth would be a next step,” said Steinman. Insulin-like growth factor-raising therapeutic agents that may be considered, which would all require caution, include Prozac®, Copaxone®, Increlex®, and recombinant human insulin-like growth factor. As a natural source of insulin-like growth factor, breast milk also will be an important consideration; an increased duration of breastfeeding is associated with a decreased incidence of autism.
The research into this theory could present an opportunity for public-private collaboration between academia and industry. In fact, if corroborated, Steinman’s theory could also point to potential risks to pregnant women and women of child-bearing age of drugs able to lower insulin-like growth factor levels, of which there are several — Somavert®, Sandostatin®, Parlodel®, and several experimental insulin-like growth factor receptor antagonists.
As well, if Steinman’s theory is confirmed by the proposed, or any related, studies, a search of gene variations could then be conducted in autistic children. This kind of information might allow genetic risk determinations in the preconception period, similar to other forms of genetic testing and counseling during the family planning stages. Genetic testing and counseling for autism may be particularly helpful to couples who start families later in life. Newborn levels of insulin-like growth factor are inversely proportional to parental age, and older mothers and fathers have a higher risk of conceiving children who will later develop symptoms of autism.
In developing the hypothesis and suggested investigation, Steinman examined insulin-like growth factor research to date in the areas of genetics, intrauterine environments, postpartum factors, and nervous system development, as well as a other related factors. Steinman believes there’s a good chance this theory will be validated, but much work remains. Steinman and his collaborators are thrilled to have identified this potential connection and hope it leads not only to the discovery of the cause of autism but also a way to detect it early, treat it, and ultimately prevent it.
After long dismissing the search for a human pheromone (pheromones are airborne chemicals which are emitted to attract the opposite sex) as folly, scientists have begun to take a second look at how human body odor influences sexual attraction. The magic scent is not some romantic elixir but the aromatic effluence of our immune system. The only trouble is we don’t give it half a chance. How do we humans announce, and excite, sexual availability? Many animals do it with their own biochemical bouquets known as pheromones. Why do bulls and horses turn up their nostrils when excited by love? Darwin pondered deep in one of his unpublished notebooks. He came to believe that natural selection designed animals to produce two, and only two, types of odors—defensive ones, like the skunk’s, and scents for territorial marking and mate attracting, like that exuded by the male musk deer and bottled by perfumers everywhere. The evaluative sniffing that mammals engage in during courtship were clues that scent is the chemical equivalent of the peacock’s plumage or the nightingale’s song; finery with which to attract mates.
In the following century, rich array of animal pheromones were documented for seals, boars, rodents, and all manner of other critters. Some of Darwin’s contemporaries embraced human uniqueness in this regard as evidence of our inevitable ascendance, as if Nature’s Plan somehow called for the evolution of a nearly naked two-legged primate with a poor sense of smell to conquer the Earth. The French physician Paul Broca—noting that primates’ social olfactory abilities are diminished compared to those of other mammals asserted that monkeys, apes, and humans represent ascending steps from four-legged sniffing beasts to sight-oriented bipeds. Monkeys, he argued, have smaller "smell brains" than other mammals, and apes’ brains are even smaller than that. Among humans, only the tribal "primitives," Broca wrote, could still attach erotic import to the bodily smells of man.
More enlightened researchers dismissed such views as racist tripe. But they still noted that humans engage in very little scent-driven socializing; compared to, say, the urine-washing displays of monkeys; during which urine is rubbed on the feet to attract mates. To make matters worse, humans seemed to lack the hardware for communicating by scent. Pheromone reception in other species is the business of two little pits (one in each nostril) known collectively as the vomeronasal organ. Few scientists claimed to have been able to locate a human vomeronasal organ. Those who did complained that the vomeronasal organ is so small that they could detect it only rarely. But most scientists, without bothering to look, simply dismissed the idea of a vomeronasal organ in humans. It’s been scientific dogma for most of this century that humans do not rely on scent to any appreciable degree, and that any vomeronasal organs found are vestigial throwbacks. Then, in the 1930s, physiologists declared that humans lack the brain part to process vomeronasal organ signals; firmly closing the book on any role for body odor in human sexual attraction. Even if we had a vomeronasal organ, the thinking was, our brains wouldn’t be able to interpret its signals.
Recent discoveries suggest, however, that the reports of our olfactory devolution have been greatly exaggerated. Some suspected as much the whole time. Smell researchers Barbara Sommerville and David Gee of the University of Leeds in England observed that smelling one another’s hands or faces is a nearly universal human greeting. The Eskimo kiss is not just a rubbing of noses but a mutual sniffing. "Only in the Western world," the researchers point out, "has it become modified to a kiss." Hands and faces may be significant choices for these formalities; they are the two most accessible concentrations of scent glands on the human body besides the ears.
Inquisitively, remembering a smell is usually difficult, yet when exposed to certain scents, many people of whom Proust is the paragon may suddenly recall a distant childhood memory in emotionally rich detail. Some aromas even affect us physiologically. Researchers exploring human olfaction have found that a faint trace of lemon significantly increases people’s perception of their own health. Lavender incense contributes to a pleasant mood, but it lowers volunteers’ mathematical abilities. A whiff of lavender and eucalyptus increases people’s respiratory rate and alertness. The scent of phenethyl alcohol (a constituent of rose oil) reduces blood pressure.
Such findings have led to the rapid development of an aromatherapy industry. Aromatherapists point to scientific findings that smell can dramatically affect our moods as evidence that therapy with aromatic oils can help buyers manage their emotional lives. Mood is demonstrably affected by scent. But scientists have found that, despite some extravagant industry promises, the attraction value in perfumes resides strictly in their pleasantness, not their sexiness. So far, at least, store-bought scent is more decoration than mood manager or love potion. A subtle "look this way" nudge to the nose, inspiring a stranger’s curiosity, or at most a smile, is all perfume advertisers can in good conscience claim for their products; not overwhelming and immediate infatuation.
Grandiose claims for the allure of a bottled smell are not new. In their haste to mass-market sexual attraction during the last century, perfumers nearly drove the gentle musk deer extinct. In Victorian England, a nice-smelling young lady with financial savvy could do a brisk business selling handkerchiefs scented with her body odor. So it should come as no surprise that when physiologists discovered a functioning vomeronasal organ inside the human nose, it was a venture capitalist intent on cashing in on manufactured human pheromone who funded the team’s research. That was in the mid 1980s. Using high-tech microscope probes that were unavailable to vomeronasal organ hunters earlier in the century, a team led by Luis Monti-Bloch of the University of Utah found a tiny pair of pits, one in each nostril, snuggled up against the septum an inch inside the nose. The pits are lined with receptor cells that fire like mad when presented with certain substances. Yet subjects report that they don’t smell a thing during such experiments. What they often do report is a warm, vague feeling of well-being. The olfactory bulb that neurophysiologists couldn’t find in the 1930s isn’t absent in human brains at all, researchers recently discovered. It’s just so enveloped by the massive frontal cortex that it’s very difficult to find. This finding, coupled with the discovery of a functional human vomeronasal organ, has ushered in a new chapter of the story of a human pheromone.
For an animal whose nose supposedly plays no role in sexual attraction or social life, human emotions are strongly moved by smells. We appear to be profoundly over-equipped with smell-producing hardware for what little sniffing we have been thought to be up to. Human sweat, urine, breath, saliva, breast milk, skin oils, and sexual secretions all contain scent-communicating chemical compounds. Zoologist Michael Stoddart, author of The Scented Ape (Cambridge University Press, 1991), points out that humans possess denser skin concentrations of scent glands than almost any other mammal. This makes little sense until one abandons the myth that humans pay little attention to the fragrant or the rancid in their day-to-day lives.
Part of the confusion may be due to the fact that not all smells register in our conscious minds. When those telltale scents were introduced to the vomeronasal organ of human subjects, they didn’t report smelling anything, but nevertheless demonstrated subtle changes in mood.
Humans possess three major types of skin glands: sebaceous glands, eccrine or sweat glands, and apocrine glands (A type of gland that found in the skin, breast, eyelid, and ear. Apocrine glands in the breast secrete fat droplets into breast milk and those in the ear help form earwax. Apocrine glands in the skin and eyelid are sweat glands. Most apocrine glands in the skin are in the armpits, the groin, and the area around the nipples of the breast. Apocrine glands in the skin are scent glands, and their secretions usually have an odor. Another type of gland called eccrine gland or simple sweat gland produces most sweat). Sebaceous glands are most common on the face and forehead but occur around all of the body’s openings, including eyelids, ears, nostrils, lips, and nipples. This placement is particularly handy, as the secretions of these glands kill potentially dangerous microorganisms. They also contain fats that keep skin supple and waterproof and, on the downside, cause acne vulgaris. Little is known, however, about how sebaceous glands contribute to human body odor.
The sweat glands exude water and salt and are non-odorous in healthy people. That leaves the third potential source of a human pheromone—the apocrine gland. Apocrine glands hold special promise as the source of smells that might affect interpersonal interactions. They do not serve any temperature-managing functions in people, as they do in other animals. They occur in dense concentrations on hands, cheeks, scalp, breast areolas, and wherever we possess body hair—and are only functional after puberty, when we begin searching for mates.
Men’s apocrine glands are larger than women’s, and they secrete most actively during times of nervousness or excitement. Waiting colonies of bacteria turn apocrine secretions into the noxious fumes that keep deodorant makers in business. Hair provides surface area from which apocrine smells can diffuse—part of the reason why hairier men smell particularly pungent. Is it any coincidence that hair at the arm pit and the genitals sprouts at puberty, when apocrine glands start producing food for our skin bacteria?
Apocrine glands exude odorous steroids known to elicit sexual behavior in mammals. Androsterone—a steroid related to the one that nearly doomed the hapless musk deer—is one such substance. Men secrete more androsterone than women do, and most men become unable to detect the stuff right around the time they start producing it themselves—at puberty. In 1986, the National Geographic Society organized the World Smell Survey to investigate whether people from all cultures experience odor in the same fashion. They distributed over a million scratch-and-sniff cards and questionnaires about subjects’ detection and perceptions of intensity of smells, from banana to the sulfur compounds added to natural gas as a warning agent. Included in the survey was the scent of human androsterone. The steroid itself is not pleasant to smell. Worldwide, those who could smell it rated it second to last in pleasantness—just ahead of the sulfur compounds put in natural gas; a foul-smelling pheromone? It’s hardly what scientists expected to find.
Despite the poor showing of androsterone in smell ratings, Karl Grammer of Austria’s Institute for Human Biology thought it might be the sought-after human pheromone and studied women’s reactions to it. He expected to find that women have a strong, favorable reaction to the smell of androsterone around ovulation, when their sense of smell becomes more acute and when they are most likely to conceive. Changes in female bodies’ estrogen levels around ovulation were suspected may change how women react to androsterone’s smell. Grammer found that women’s reactions to androsterone indeed change around ovulation, but not in the manner he expected. Instead of attraction, Grammer’s ovulating volunteers shrugged their shoulders and reported ambivalence. Androsterone, it seems, offers little hope to men looking for a $19.95 solution to their dating slumps.
The empirical proof of odor’s effect on human sexual attraction came out of left field. Medical geneticists studying inheritance rules for the immune system; not smell physiologists, made a series of crucial discoveries that nobody believed were relevant to human mate preferences—at first. Research on tissue rejection in organ transplant surgery patients led to the discovery that the body recognizes an alien presence; whether a virus or a surgically implanted kidney because the body’s own cells are coated with proteins that our immune system recognizes as "self." But the immune system gets a lot more subtle about recognizing "nonself" intruders. It can recognize specific types of disease organisms, attach protein identifiers to them, and muster antibodies designed specifically for destroying that particular disease and it can "remember" that particular invader years later, sending out specific antibodies to it.
A segment of our DNA called the major histocompatibility complex codes for some of these disease-detecting structures, which function as the immune system’s eyes. When a disease is recognized, the immune system’s teeth—the killer T cells—are alerted, and they swarm the intruders, smothering them with destructive enzymes. Unlike many genes, which have one or two alternative versions like the genes that code for attached or unattached ear lobes, major histocompatibility complex genes have dozens of alternatives and unlike earlobe genes, in which the version inherited from one parent dominates so that the version inherited from the other parent is not expressed, major histocompatibility complex genes are "co-dominant." This means that if a lab mouse inherits a version of a major histocompatibility complex gene for resistance to Disease A from its mother and a version lending resistance to Disease B from its father, that mouse will be able to resist both diseases.
When a female mouse is offered two suitors in mate choice trials, she inevitably chooses to mate with the one whose major histocompatibility complex genes least overlap with her own. It turns out that female mice evaluate males’ major histocompatibility complex profile by sniffing their urine. The immune system creates scented proteins that are unique to every version of each major histocompatibility complex gene. These immune byproducts are excreted from the body with other used-up chemicals, allowing a discerning female to sniff out exactly how closely related to her that other mouse is.
By choosing major histocompatibility complex dissimilar mates, a female mouse makes sure that she doesn’t inbreed. She also secures a survival advantage for her offspring by assuring that they will have a wider range of disease resistance than they would had she mated with her brother. It’s not that she seeks out diverse major histocompatibility complex genes for her young on purpose, of course. Ancestral females who preferred the smell of closely related males were simply outrun through evolutionary time by females who preferred the scent of unrelated sires.
Since humans show little interest in one another’s urine, few researchers thought that the story of major histocompatibility complex in rodent attraction could shed light on human interactions. But then someone made an eyebrow-raising discovery: Human volunteers can discriminate between mice that differ genetically only in their major histocompatibility complex. If human noses could detect small differences in the immune systems of mice by giving the critters a sniff, excited researchers realized, we may well be able to detect the aromatic byproducts of the immune system in human body odor as well.
A team led by Claus Wedekind at the University of Bern in Switzerland decided to see whether major histocompatibility complex differences in men’s apocrine gland secretions affected women’s ratings on male smells. The team recruited just fewer than 100 college students. Males and females were sought from different schools, to reduce the chances that they knew each other. The men were given untreated cotton T-shirts to wear as they slept alone for two consecutive nights. They were told not to eat spicy foods; not to use deodorants, cologne, or perfumed soaps; and to avoid smoking, drinking, and sex during the two-day experiment. During the day, their sweaty shirts were kept in sealed plastic containers and then came the big smell test. For two weeks prior, women had used a nasal spray to protect the delicate mucous membranes lining the nose. Around the time they were ovulating when their sense of smell is enhanced, the women were put alone in a room and presented with boxes containing the male volunteers’ shirts. First they sniffed a new, unworn shirt to control for the scent of the shirts themselves. Then the women were asked to rate each man’s shirt for "sexiness," "pleasantness," and "intensity of smell."
It was found; by Wedekind and his team that how women rate a man’s body odor pleasantness and sexiness depends upon how much of their major histocompatibility complex profile is shared. Overall, women prefer those scents exuded by men whose major histocompatibility complex profiles varied the most from their own. Hence, any given man’s odor could be pleasingly alluring to one woman, yet an offensive turnoff to another. Raters said that the smells they preferred reminded them of current or ex-lovers about twice as often as did the smells of men who have major histocompatibility complex profiles similar to their own, suggesting that smell had played a role in past decisions about who to date. Major histocompatibility complex similar men’s smells were more often described as being like a brother’s or father’s body odor… as would be expected if the components of smell being rated are major histocompatibility complex determined.
Somewhat more surprising is that women’s evaluations of body odor intensities did not differ between major histocompatibility complex similar and major histocompatibility complex dissimilar men. Body scent for major histocompatibility complex dissimilar men was rated as less sexy and less pleasant the stronger it was, but intensity did not affect the women’s already low ratings for major histocompatibility complex similar men’s smells. That strong odor turned raters off even with major histocompatibility complex dissimilar men may be due to the fact odor is a useful indicator of disease. From diabetes to viral infection to schizophrenia, unusually sweet or strong body odors are a warning cues that ancestral female in search of good genes for their offspring may have been designed to heed. In the case of schizophrenia, the issue is confounded—while some schizophrenics do actually have an unusually sweet smell, many suffer from delusions of foul smells emanating from their bodies.
Nobody yet knows what roles major histocompatibility complex may play in male evaluations of female attractiveness. Females’ superior sense of smell, however, may well be due to their need to more carefully evaluate a potential mates merits—a poor mate choice for male ancestors may have meant as little as a few minutes wasted, whereas a human female’s mistake could result in a nine-month-long "morning after" and a child unlikely to survive.
Perfumers who really want to provide that sexy allure to their male customers will apparently need to get a genetic fingerprint of the special someone before they can tailor a scent that she will find attractive. But before men contemplate fooling women in this way, they should consider the possible consequences. The Swiss researchers found that women taking oral contraceptives; which block conception by tricking the body into thinking it is pregnant reported reversed preferences, liking more the smells that reminded them of home and kin. Since the Pill reverses natural preferences, a woman may feel attracted to men she wouldn’t normally notice if she were not on birth control—men who have similar major histocompatibility complex profiles.
The effects of such evolutionary novel mate choices can go well beyond the bewilderment of a wife who stops taking her contraceptive pills and notices her husband’s "newly" foul body odor. Couples experiencing difficulty conceiving a child—even after several attempts at tubal embryo transfer—share significantly more of their major histocompatibility complex than do couples who conceive more easily. These couples’ grief is not caused by either partner’s infertility, but to an unfortunate combination of otherwise viable genes.
Doctors have known since the mid-1980s that couples suffering repeated spontaneous abortions tend to share more of their major histocompatibility complex than couples for whom pregnancies are carried to term and even when major histocompatibility complex similar couples do successfully bring a pregnancy to term, their babies are often underweight. The Swiss team believes that major histocompatibility complex related pregnancy problems in humans are too widespread to be due to inbreeding alone. They argue that in-couple infertility problems are due to strategic, unconscious "decisions" made by women bodies to curtail investment in offspring with inferior immune systems; offspring unlikely to have survived to adulthood in the environments of our evolutionary past.
When Broca and other social Darwinists pointed out that "uncivilized races" were more sensitive to body odor, they may have been correct—insofar as Europeans tend to go to greater lengths to perfume and wash away their natural scents. But this is hardly evidence of European superiority over "less evolved" peoples, as Broca insisted. Paying careful attention to the health of others and their suitability as sires to one’s offspring in the disease-rich tropics, whose cultures Broca derided, actually makes exceedingly good sense.
Perfume; daily soapy showers; convenient contraceptive pills—all have their charms. But they also may be short-circuiting our own built-in means of mate choice, adaptations shaped to our unique needs by millions of years of ancestral adversities. The existence of couples who long for children they cannot have indicates that the Western dismissal of body scent is scarcely benign. Those who find offensive the notion that animal senses play a role in their attraction to a partner need not worry. As the role of smell in human affairs yields to understanding, we see not that we are less human but that our tastes and emotions are far more complex and sophisticated than anyone ever imagined.
How to smell a mate? How does body odor affect a woman’s sexiness?
Scientists don’t know for sure, but they do know that a man’s allure depends in part on how many immune system genes he shares with a potential mate. Since it’s known that women can detect genetic compatibility by smell—it’s not that men can’t but that so far no one knows—the onus is on females to sniff out a suitable squire. Choosing a genetically compatible partner can be difficult in today’s perfume rich postindustrial jungle, and getting your immune system genes profiled can be expensive. Before you run to a doctor for blood work to see whether your mate is a suitable match—and sire for your future children—try listening to your nose. Unfortunately, the sniff test will only work if you’re not taking birth control pills.
Declare a deception-free day for the nostrils. Have your beau shower with fragrance-free soap and wear clean cotton clothing for a day, away from smokers and the perfumed masses. Be sure you don’t have a cold, and that you yourself haven’t been around smokers for a few days. After he spends a day and a night in his cotton clothes, before he tosses them in the direction of the hamper, wrestle them from him and have a "smelldown." Make it a romantic experience. If your man’s shirt doesn’t offend, you should be safe. Find the scent alluring or sexy? Even better! That attraction is nature’s way of telling you he’s a safe contributor to your offspring’s genetic ensemble. If your man’s odor reminds you of your father or of a brother, you may want to consider getting in touch with your doctor and ask about genetic tests before trying to conceive a child. Tell the doctor you’re concerned that you may share a close major histocompatibility complex or human leukocyte antigen, is a technical tag for human major histocompatibility complex. Meanwhile, a deceptively pleasing gift of cologne might be in order. Genetic incompatibility is not the only reason you may find his odor offensive. Does his body scent seem unusually intense? He might have a medical condition that explains the smell. Ask him to bring it up at his next medical checkup. A very sweet scent is sometimes evidence of diabetes or schizophrenia—both of which appear to be heritable. It is wise to discuss these issues with each other, and with a doctor, before having kids. Before you decide that your relationship stinks, check your mate’s diet; a taste for spicy foods or overindulgence in garlic can cause strong body odors. If your mate still offends, don’t head for the hills just yet. Some clothing detergents can prove to be a bad mix with a fellow’s scent. Ask that the next time he visits the laundry, he change brands—and give the stinker a second chance!
An embryo has no rights. Rights do not pertain to a potential, only to an actual being. A child cannot acquire any rights until it is born. The living takes precedence over the not-yet-living or the unborn. Abortion is a moral right; which should be left to the sole discretion of the woman involved; morally, nothing other than her wish in the matter is to be considered. Who can conceivably have the right to dictate to her what disposition she is to make of the functions of her own body?
Never mind the vicious nonsense of claiming that an embryo has a “right to life.” A piece of protoplasm has no rights—and no life in the human sense of the term. One may argue about the later stages of a pregnancy, but the essential issue concerns only the first three months. To equate a potential with an actual, is vicious; to advocate the sacrifice of the latter to the former, is unspeakable. Observe that by ascribing rights to the unborn, i.e., the nonliving, the anti-abortionists obliterate the rights of the living, the right of young people to set the course of their own lives. The task of raising a child is a tremendous, lifelong responsibility, which no one should undertake unwittingly or unwillingly. Procreation is not a duty. Human beings are not stock-farm animals. For conscientious persons, an unwanted pregnancy is a disaster; to oppose its termination is to advocate sacrifice, not for the sake of anyone’s benefit, but for the sake of misery qua misery, for the sake of forbidding happiness and fulfillment to living human beings.
If any among you are confused or taken in by the argument that the cells of an embryo are living human cells, remember that so are all the cells of your body, including the cells of your skin, your tonsils, or your ruptured appendix—and that cutting them is murder, according to the notions of that proposed law. Remember also that a potentiality is not the equivalent of an actuality and that a human being’s life begins at birth. The question of abortion involves much more than the termination of a pregnancy. It is a question of the entire life of the parents. Parenthood is an enormous responsibility. It is an impossible responsibility for young people who are ambitious and struggling, but poor; particularly if they are intelligent and conscientious enough not to abandon their child on doorstep or to surrender it to adoption. For such young people, pregnancy is a death sentence. Parenthood would force them to give up their future, and condemn them to a life of hopeless drudgery, of slavery to a child’s physical and financial needs. The situation of an unwed mother, abandoned by her lover, is even worse.
I cannot quite imagine the state of mind of a person who would wish to condemn a fellow human being to such a horror. I cannot project the degree of hatred required to make those women run around in crusades against abortion. Hatred is what they certainly project, not love for the embryo, which is a piece of nonsense no one could experience, but hatred, a virulent hatred for an unnamed object. Judging by the degree of those women’s intensity, I would say that it is an issue of self-esteem and that their fear is metaphysical. Their hatred is directed against human beings as such, against the mind, against reason, against ambition, against success, against love, against any value that brings happiness to human life. In compliance with the dishonesty that dominates today’s intellectual field, they call themselves “pro-life.” By what right does anyone claim the power to dispose of the lives of others and to dictate their personal choices? A proper, philosophically valid definition of man as “a rational animal,” would not permit anyone to ascribe the status of “person” to a few human cells.
Reduce Psychotropics in Early Pregnancy
Psychotropic medication during early pregnancy; runs risk of miscarriage and perinatal death.
Women taking antidepressant or anti-anxiety medications during early pregnancy have high risks of non-live pregnancy outcomes, although the contribution of the underlying illnesses to these risks remains unclear. The study consists of impacts of antenatal depression and anxiety and of commonly prescribed treatments on the risks of non-live pregnancy outcomes.
The study method included identifying all pregnancies and their outcome: live birth, perinatal death, miscarriage or termination among women aged 15–45 years between 1990 and 2009 from a large primary care database in the United Kingdom. Women were grouped according to whether they had no history of depression and anxiety, a diagnosis of such illness prior to pregnancy, illness during pregnancy and illness during pregnancy with use of medication (stratified by medication type). Multinomial logistic regression models were used to compare risks of non-live outcomes among these groups, adjusting for major socio-demographic and lifestyle characteristics.
Outcome of the study: Among 512,574 pregnancies in 331,414 women, those with antenatal drug exposure showed the greatest increased risks for all non-live pregnancy outcomes, relative to those with no history of depression or anxiety, although women with prior; but not, currently medicated illness also showed modest increased risks. Compared with un-medicated antenatal morbidity, there was weak evidence of an excess risk in women taking tricyclic antidepressants, and stronger evidence for other medications.
Now it is inferred that women with depression or anxiety have higher risks of miscarriage, perinatal death and decisions to terminate a pregnancy if prescribed psychotropic medication during early pregnancy than if not. Although, underlying disease severity could also play a role, avoiding or reducing use of these drugs during early pregnancy may be advisable.