Late night snacking increases your risk of heart disease

When it comes to protecting yourself from heart disease, I’m sure you take all the obvious steps like exercising regularly, avoiding low-fat sugar-laden foods, not smoking and following a diet rich in fresh fruit, veg and healthy lean animal proteins.

Of course, we are all human so it is only normal to sometimes slip up and indulge a little bit. But if there is one indulgence you need to avoid, then it is those cheeky late night snacks.

Snack attack

It’s late at night… it’s way past your bedtime… or you’ve woken up in the middle of the night… you are restless… tossing and turning… finally, you stumble to the fridge.

Once that door opens and that little light turns on, the grazing begins… anything goes!

However, according to a new study, you should really avoid those midnight snack attacks because eating during the night can up your chances of heart disease.

Researchers fed a group of rats at the beginning of their rest period and at the beginning of their active phase, and then they measured their levels of blood fats (triglycerides) after each meal.

We know that in humans, having high levels of triglycerides in the blood is a risk factor for heart disease.

The researchers found that the rats’ triglycerides spiked more drastically when they ate at the start of their rest period, compared to when they ate at the start of their active phase.

This suggests that eating when they should have been resting disturbed the rats’ natural biological clock.

Of course, humans aren’t lab animals, but humans and rats are actually very similar in how our bodies respond to stimulants.

Previous studies have shown that when you ignore your biological clock and shovel in midnight snacks, you can add pounds to your waistline… elevate your blood pressure… and even make it harder for your brain to form new memories.

It also makes perfect sense that eating too late could spike your triglycerides — because your muscles and tissues don’t soak up these fats for fuel when your internal clock signals that it’s rest time.

So, the next time you wake up in the wee hours of the morning don’t find comfort in the fridge.

If hunger is driving you, try eating a high-protein dinner with lots of fibre to keep you feeling full until morning.

But if your snacking sessions are fuelled by anxiety, taking a warm bath or a hot shower can calm your nerves and help you sleep like a baby.

Female infertility

Infertility is defined as trying to get pregnant (with frequent intercourse) for at least a year with no success. Female infertility, male infertility or a combination of the two affects millions of couples in the United States. An estimated 10 to 18 percent of couples have trouble getting pregnant or having a successful delivery.

Infertility results from female factors about one-third of the time and male factors about one-third of the time. The cause is either unknown or a combination of male and female factors in the remaining cases.

Female infertility causes can be difficult to diagnose. There are many available treatments, which will depend on the cause of infertility. Many infertile couples will go on to conceive a child without treatment. After trying to get pregnant for two years, about 95 percent of couples successfully conceive.

Symptoms

The main symptom of infertility is the inability to get pregnant. A menstrual cycle that’s too long (35 days or more), too short (less than 21 days), irregular or absent can mean that you’re not ovulating. There may be no other outward signs or symptoms.

When to see a doctor

When to seek help sometimes depends on your age:

• Up to age 35, most doctors recommend trying to get pregnant for at least a year before testing or treatment.
• If you’re between 35 and 40, discuss your concerns with your doctor after six months of trying.
• If you’re older than 40, your doctor may want to begin testing or treatment right away.

Your doctor may also want to begin testing or treatment right away if you or your partner has known fertility problems, or if you have a history of irregular or painful periods, pelvic inflammatory disease, repeated miscarriages, prior cancer treatment, or endometriosis.

Each of these factors is essential to become pregnant:

• You need to ovulate. To get pregnant, your ovaries must produce and release an egg, a process known as ovulation. Your doctor can help evaluate your menstrual cycles and confirm ovulation.
• Your partner needs sperm. For most couples, this isn’t a problem unless your partner has a history of illness or surgery. Your doctor can run some simple tests to evaluate the health of your partner’s sperm.
• You need to have regular intercourse. You need to have regular sexual intercourse during your fertile time. Your doctor can help you better understand when you’re most fertile.
• You need to have open fallopian tubes and a normal uterus. The egg and sperm meet in the fallopian tubes, and the embryo needs a healthy uterus in which to grow.

For pregnancy to occur, every step of the human reproduction process has to happen correctly. The steps in this process are:

• One of the two ovaries releases a mature egg.
• The egg is picked up by the fallopian tube.
• Sperm swim up the cervix, through the uterus and into the fallopian tube to reach the egg for fertilization.
• The fertilized egg travels down the fallopian tube to the uterus.
• The fertilized egg implants and grows in the uterus.

In women, a number of factors can disrupt this process at any step. Female infertility is caused by one or more of the factors below.

Ovulation disorders

Ovulation disorders, meaning you ovulate infrequently or not at all, account for infertility in about 1 in 4 infertile couples. Problems with the regulation of reproductive hormones by the hypothalamus or the pituitary gland, or problems in the ovary, can cause ovulation disorders.

• Polycystic ovary syndrome (PCOS). PCOS causes a hormone imbalance, which affects ovulation. PCOS is associated with insulin resistance and obesity, abnormal hair growth on the face or body, and acne. It’s the most common cause of female infertility.
• Hypothalamic dysfunction. Two hormones produced by the pituitary gland are responsible for stimulating ovulation each month — (FSH) and luteinizing hormone (LH). Excess physical or emotional stress, a very high or very low body weight, or a recent substantial weight gain or loss can disrupt production of these hormones and affect ovulation. Irregular or absent periods are the most common signs.
• Premature ovarian failure. Also called primary ovarian insufficiency, this disorder is usually caused by an autoimmune response or by premature loss of eggs from your ovary (possibly from genetics or chemotherapy). The ovary no longer produces eggs, and it lowers estrogen production in women under the age of 40.
• Too much prolactin. The pituitary gland may cause excess production of prolactin (hyperprolactinemia), which reduces estrogen production and may cause infertility. Usually related to a pituitary gland problem, this can also be caused by medications you’re taking for another disease.

Damage to fallopian tubes (tubal infertility)

Damaged or blocked fallopian tubes keep sperm from getting to the egg or block the passage of the fertilized egg into the uterus. Causes of fallopian tube damage or blockage can include:

• Pelvic inflammatory disease, an infection of the uterus and fallopian tubes due to chlamydia, gonorrhea or other sexually transmitted infections
• Previous surgery in the abdomen or pelvis, including surgery for ectopic pregnancy, in which a fertilized egg implants and develops in a fallopian tube instead of the uterus
• Pelvic tuberculosis, a major cause of tubal infertility worldwide, although uncommon in the United States

Endometriosis

Endometriosis occurs when tissue that normally grows in the uterus implants and grows in other locations. This extra tissue growth — and the surgical removal of it — can cause scarring, which may block fallopian tubes and keep an egg and sperm from uniting.

Endometriosis can also affect the lining of the uterus, disrupting implantation of the fertilized egg. The condition also seems to affect fertility in less-direct ways, such as damage to the sperm or egg.

Uterine or cervical causes

Several uterine or cervical causes can impact fertility by interfering with implantation or increasing the likelihood of a miscarriage:

• Benign polyps or tumors (fibroids or myomas) are common in the uterus. Some can block fallopian tubes or interfere with implantation, affecting fertility. However, many women who have fibroids or polyps do become pregnant.
• Endometriosis scarring or inflammation within the uterus can disrupt implantation.
• Uterine abnormalities present from birth, such as an abnormally shaped uterus, can cause problems becoming or remaining pregnant.
• Cervical stenosis, a narrowing of the cervix, can be caused by an inherited malformation or damage to the cervix.
• Sometimes the cervix can’t produce the best type of mucus to allow the sperm to travel through the cervix into the uterus.

Unexplained infertility

Sometimes, the cause of infertility is never found. A combination of several minor factors in both partners could cause unexplained fertility problems. Although it’s frustrating to get no specific answer, this problem may correct itself with time. But, you shouldn’t delay treatment for infertility.

Risk factors

Certain factors may put you at higher risk of infertility, including:

• Age. The quality and quantity of a woman’s eggs begin to decline with increasing age. In the mid-30s, the rate of follicle loss speeds, resulting in fewer and poorer quality eggs. This makes conception more difficult, and increases the risk of miscarriage.
• Smoking. Besides damaging your cervix and fallopian tubes, smoking increases your risk of miscarriage and ectopic pregnancy. It’s also thought to age your ovaries and deplete your eggs prematurely. Stop smoking before beginning fertility treatment.
• Weight. Being overweight or significantly underweight may affect normal ovulation. Getting to a healthy body mass index (BMI) may increase the frequency of ovulation and likelihood of pregnancy.
• Sexual history. Sexually transmitted infections such as chlamydia and gonorrhea can damage the fallopian tubes. Having unprotected intercourse with multiple partners increases your risk of a sexually transmitted infection that may cause fertility problems later.
• Alcohol. Stick to moderate alcohol consumption of no more than one alcoholic drink per day.

Prevention

If you’re a woman thinking about getting pregnant soon or in the future, you may improve your chances of having normal fertility if you:

• Maintain a normal weight. Overweight and underweight women are at increased risk of ovulation disorders. If you need to lose weight, exercise moderately. Strenuous, intense exercise of more than five hours a week has been associated with decreased ovulation.
• Quit smoking. Tobacco has multiple negative effects on fertility, not to mention your general health and the health of a fetus. If you smoke and are considering pregnancy, quit now.
• Avoid alcohol. Heavy alcohol use may lead to decreased fertility. And any alcohol use can affect the health of a developing fetus. If you’re planning to become pregnant, avoid alcohol, and don’t drink alcohol while you’re pregnant.
• Reduce stress. Some studies have shown that couples experiencing psychological stress had poorer results with infertility treatment. If you can, find a way to reduce stress in your life before trying to become pregnant.
• Limit caffeine. Research suggests that limiting caffeine intake to less than 200 milligrams a day shouldn’t affect your ability to get pregnant. That’s about one to two cups of 6 to 8 ounces of coffee per day.
  

  Diagnosis

  If you’ve been unable to conceive within a reasonable period of time, seek help from your doctor for evaluation and treatment of infertility.
  Fertility tests may include:
  • Ovulation testing. An at-home, over-the-counter ovulation prediction kit detects the surge in luteinizing hormone (LH) that occurs before ovulation. A blood test for progesterone — a hormone produced after ovulation — can also document that you’re ovulating. Other hormone levels, such as prolactin, also may be checked.
  • Hysterosalpingography. During hysterosalpingography (his-tur-o-sal-ping-GOG-ruh-fee), X-ray contrast is injected into your uterus and an X-ray is taken to detect abnormalities in the uterine cavity. The test also determines whether the fluid passes out of the uterus and spills out of your fallopian tubes. If abnormalities are found, you’ll likely need further evaluation. In a few women, the test itself can improve fertility, possibly by flushing out and opening the fallopian tubes.
  • Ovarian reserve testing. This testing helps determine the quality and quantity of eggs available for ovulation. Women at risk of a depleted egg supply — including women older than 35 — may have this series of blood and imaging tests.
  • Other hormone testing. Other hormone tests check levels of ovulatory hormones as well as thyroid and pituitary hormones that control reproductive processes.
  • Imaging tests. A pelvic ultrasound looks for uterine or fallopian tube disease. Sometimes a hysterosonography (his-tur-o-suh-NOG-ruh-fee) is used to see details inside the uterus that can’t be seen on a regular ultrasound.
  Depending on your situation, rarely your testing may include:
  • Other imaging tests. Depending on your symptoms, your doctor may request a hysteroscopy to look for uterine or fallopian tube disease.
  • Laparoscopy. This minimally invasive surgery involves making a small incision beneath your navel and inserting a thin viewing device to examine your fallopian tubes, ovaries and uterus. A laparoscopy may identify endometriosis, scarring, blockages or irregularities of the fallopian tubes, and problems with the ovaries and uterus.
  • Genetic testing. Genetic testing helps determine whether there’s a genetic defect causing infertility.

  Treatment

  Infertility treatment depends on the cause, your age, how long you’ve been infertile and personal preferences. Because infertility is a complex disorder, treatment involves significant financial, physical, psychological and time commitments.
  Although some women need just one or two therapies to restore fertility, it’s possible that several different types of treatment may be needed.
  Treatments can either attempt to restore fertility through medication or surgery, or help you get pregnant with sophisticated techniques.

  Fertility restoration: Stimulating ovulation with fertility drugs

  Fertility drugs regulate or stimulate ovulation. Fertility drugs are the main treatment for women who are infertile due to ovulation disorders.
  Fertility drugs generally work like the natural hormones — follicle-stimulating hormone (FSH) and luteinizing hormone (LH) — to trigger ovulation. They’re also used in women who ovulate to try to stimulate a better egg or an extra egg or eggs. Fertility drugs may include:
  • Clomiphene citrate. Clomiphene (Clomid) is taken by mouth and stimulates ovulation by causing the pituitary gland to release more FSH and LH, which stimulate the growth of an ovarian follicle containing an egg.
  • Gonadotropins. Instead of stimulating the pituitary gland to release more hormones, these injected treatments stimulate the ovary directly to produce multiple eggs. Gonadotropin medications include human menopausal gonadotropin or hMG(Menopur) and FSH (Gonal-F, Follistim AQ, Bravelle). Another gonadotropin, human chorionic gonadotropin (Ovidrel, Pregnyl), is used to mature the eggs and trigger their release at the time of ovulation. Concerns exist that there’s a higher risk of conceiving multiples and having a premature delivery with gonadotropin use.
  • Metformin. Metformin (Glucophage, others) is used when insulin resistance is a known or suspected cause of infertility, usually in women with a diagnosis of PCOS. Metformin helps improve insulin resistance, which can improve the likelihood of ovulation.
  • Letrozole. Letrozole (Femara) belongs to a class of drugs known as aromatase inhibitors and works in a similar fashion to clomiphene. Letrozole may induce ovulation. However, the effect this medication has on early pregnancy isn’t yet known, so it isn’t used for ovulation induction as frequently as others.
  • Bromocriptine. Bromocriptine (Cycloset), a dopamine agonist, may be used when ovulation problems are caused by excess production of prolactin (hyperprolactinemia) by the pituitary gland.

  Risks of fertility drugs

  Using fertility drugs carries some risks, such as:
  • Pregnancy with multiples. Oral medications carry a fairly low risk of multiples (less than 10 percent) and mostly a risk of twins. Your chances increase up to 30 percent with injectable medications. Injectable fertility medications also carry the major risk of triplets or more (higher order multiple pregnancy).Generally, the more fetuses you’re carrying, the greater the risk of premature labor, low birth weight and later developmental problems. Sometimes adjusting medications can lower the risk of multiples, if too many follicles develop.
  • Ovarian hyperstimulation syndrome (OHSS). Injecting fertility drugs to induce ovulation can cause OHSS, which causes swollen and painful ovaries. Signs and symptoms usually go away without treatment, and include mild abdominal pain, bloating, nausea, vomiting and diarrhea.If you become pregnant, however, your symptoms might last several weeks. Rarely, it’s possible to develop a more-severe form of OHSS that can also cause rapid weight gain, enlarged painful ovaries, fluid in the abdomen and shortness of breath.
  • Long-term risks of ovarian tumors. Most studies of women using fertility drugs suggest that there are few if any long-term risks. However, a few studies suggest that women taking fertility drugs for 12 or more months without a successful pregnancy may be at increased risk of borderline ovarian tumors later in life.Women who never have pregnancies have an increased risk of ovarian tumors, so it may be related to the underlying problem rather than the treatment. Since success rates are typically higher in the first few treatment cycles, re-evaluating medication use every few months and concentrating on the treatments that have the most success appear to be appropriate.

  Fertility restoration: Surgery

  Several surgical procedures can correct problems or otherwise improve female fertility. However, surgical treatments for fertility are rare these days due to the success of other treatments. They include:
  • Laparoscopic or hysteroscopic surgery. These surgeries can remove or correct abnormalities to help improve your chances of getting pregnant. Surgery might involve correcting an abnormal uterine shape, removing endometrial polyps and some types of fibroids that misshape the uterine cavity, or removing pelvic or uterine adhesions.
  • Tubal surgeries. If your fallopian tubes are blocked or filled with fluid (hydrosalpinx), your doctor may recommend laparoscopic surgery to remove adhesions, dilate a tube or create a new tubal opening. This surgery is rare, as pregnancy rates are usually better with IVF. For hydrosalpinx, removal of your tubes (salpingectomy) or blocking the tubes close to the uterus can improve your chances of pregnancy with IVF.

  Reproductive assistance

  The most commonly used methods of reproductive assistance include:

  Hysterosalpingography

  • Intrauterine insemination (IUI). During IUI, millions of healthy sperm are placed inside the uterus close to the time of ovulation.
  • Assisted reproductive technology. This involves retrieving mature eggs from a woman, fertilizing them with a man’s sperm in a dish in a lab, then transferring the embryos into the uterus after fertilization. IVF is the most effective assisted reproductive technology. An IVF cycle takes several weeks and requires frequent blood tests and daily hormone injections.

Ectopic Pregnancy

Ectopic pregnancy is the result of a flaw in human reproductive physiology that allows the conceptus to implant and mature outside the endometrial cavity (see the image below), which ultimately ends in the death of the fetus. Without timely diagnosis and treatment, ectopic pregnancy can become a life-threatening situation. 

Signs and symptoms

The classic clinical triad of ectopic pregnancy is as follows:

• Abdominal pain
• Amenorrhea
• Vaginal bleeding

Unfortunately, only about 50% of patients present with all 3 symptoms.

Patients may present with other symptoms common to early pregnancy (eg, nausea, breast fullness). The following symptoms have also been reported:

• Painful fetal movements (in the case of advanced abdominal pregnancy)
• Dizziness or weakness
• Fever
• Flulike symptoms
• Vomiting
• Syncope
• Cardiac arrest

The presence of the following signs suggests a surgical emergency:

• Abdominal rigidity
• Involuntary guarding
• Severe tenderness
• Evidence of hypovolemic shock (eg, orthostatic blood pressure changes, tachycardia)

Diagnosis

Serum β-HCG levels

In a normal pregnancy, the β-HCG level doubles every 48-72 hours until it reaches 10,000-20,000mIU/mL. In ectopic pregnancies, β-HCG levels usually increase less. Mean serum β-HCG levels are lower in ectopic pregnancies than in healthy pregnancies.

No single serum β-HCG level is diagnostic of an ectopic pregnancy. Serial serum β-HCG levels are necessary to differentiate between normal and abnormal pregnancies and to monitor resolution of ectopic pregnancy once therapy has been initiated.

The discriminatory zone of β-HCG (ie, the level above which an imaging scan should reliably visualize a gestational sac within the uterus in a normal intrauterine pregnancy) is as follows:

• 1500-1800 mIU/mL with transvaginal ultrasonography, but up to 2300 mIU/mL with multiple gestates [2]
• 6000-6500 mIU/mL with abdominal ultrasonography

Absence of an intrauterine pregnancy on a scan when the β-HCG level is above the discriminatory zone represents an ectopic pregnancy or a recent abortion.

Ultrasonography

Ultrasonography is probably the most important tool for diagnosing an extrauterine pregnancy.

Visualization of an intrauterine sac, with or without fetal cardiac activity, is often adequate to exclude ectopic pregnancy. [3]

Transvaginal ultrasonography, or endovaginal ultrasonography, can be used to visualize an intrauterine pregnancy by 24 days post ovulation or 38 days after the last menstrual period (about 1 week earlier than transabdominal ultrasonography). An empty uterus on endovaginal ultrasonographic images in patients with a serum β-HCG level greater than the discriminatory cut-off value is an ectopic pregnancy until proved otherwise.

Color-flow Doppler ultrasonography improves the diagnostic sensitivity and specificity of transvaginal ultrasonography, especially in cases in which a gestational sac is questionable or absent.

Laparoscopy

Laparoscopy remains the criterion standard for diagnosis; however, its routine use on all patients suspected of ectopic pregnancy may lead to unnecessary risks, morbidity, and costs. Moreover, laparoscopy can miss up to 4% of early ectopic pregnancies.

Laparoscopy is indicated for patients who are in pain or hemodynamically unstable.

Management

Therapeutic options in ectopic pregnancy are as follows:

• Expectant management
• Methotrexate
• Surgery

Expectant management

Candidates for successful expectant management should be asymptomatic and have no evidence of rupture or hemodynamic instability. Candidates should demonstrate objective evidence of resolution (eg, declining β-HCG levels).

Close follow-up and patient compliance are of paramount importance, as tubal rupture may occur despite low and declining serum levels of β-HCG.

Methotrexate

Methotrexate is the standard medical treatment for unruptured ectopic pregnancy. A single-dose IM injection is the more popular regimen. The ideal candidate should have the following:

• Hemodynamic stability
• No severe or persisting abdominal pain
• The ability to follow up multiple times
• Normal baseline liver and renal function test results

Absolute contraindications to methotrexate therapy include the following:

• Existence of an intrauterine pregnancy
• Immunodeficiency
• Moderate to severe anemia, leukopenia, or thrombocytopenia
• Sensitivity to methotrexate
• Active pulmonary or peptic ulcer disease
• Clinically important hepatic or renal dysfunction
• Breastfeeding
• Evidence of tubal rupture

Surgical treatment

Laparoscopy has become the recommended surgical approach in most cases. Laparotomy is usually reserved for patients who are hemodynamically unstable or for patients with cornual ectopic pregnancies; it also is a preferred method for surgeons inexperienced in laparoscopy and in patients in whom a laparoscopic approach is difficult.

Candida Albicans Infection

Human immunodeficiency virus

Could a bacterium found in milk trigger rheumatoid arthritis?

New research suggests that a bacterium found in cow’s milk and beef may lead to rheumatoid arthritis in people who are already genetically predisposed. The bacterium may be a common trigger for both rheumatoid arthritis and Crohn’s disease.

A bacterium found in milk may trigger rheumatoid arthritis in genetically predisposed people, suggests new research.

Rheumatoid arthritis is an inflammatory disease that affects more than 1.3 million adults — the majority of whom are women — in the United States.

Crohn’s disease is also an inflammatory disease, and the Crohn’s and Colitis Foundation say that it affects up to 780,000 U.S. adults.

What do these two diseases have in common, apart from being characterized by inflammation? Quite a lot, actually, according to new researchrecently published in the journal Frontiers in Cellular and Infection Microbiology.

Both of these conditions share a similar genetic background and are often treated with similar immunosuppressants, because both illnesses are autoimmune disorders.

These similarities intrigued the authors of the new research, who are: Saleh Naser, who is an infectious disease specialist at the University of Central Florida (UCF) in Orlando; Dr. Shazia Bég, who is a rheumatologist at UCF’s physician practice; and Robert Sharp, who is a Ph.D. candidate in biomedical sciences at UCF’s medical school.

“Here,” says Naser, “you have two inflammatory diseases, one affects the intestine and the other affects the joints, and both share the same genetic defect and [are] treated with the same drugs. Do they have a common trigger? That was the question we raised and set out to investigate.”

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In previous research, Naser had already discovered a link between the bacterium Mycobacterium avium subspecies paratuberculosis (MAP) and Crohn’s disease, so the question of whether MAP was also somehow connected with rheumatoid arthritis followed naturally.

In fact, Naser is currently involved in a clinical trial investigating whether or not Crohn’s disease can be treated with antibiotics. Thus, if MAP proves to be present in rheumatoid arthritis as well, this condition may also be treatable with antibiotics designed to specifically target this bacterium.

Gene mutation plus MAP means higher risk

The researchers analyzed clinical samples from 100 people with rheumatoid arthritis. Of these, 78 percent had a genetic mutation that they shared with people with Crohn’s disease: the PTPN2/22 gene.

Of the people with rheumatoid arthritis with this genetic mutation, 40 percent also had MAP.

“We believe that individuals born with this genetic mutation and who are later exposed to MAP through consuming contaminated milk or meat from infected cattle are at a higher risk of developing rheumatoid arthritis.”

“We don’t know the cause of rheumatoid arthritis, so we’re excited that we have found this association,” Bég says. “But there is still a long way to go.”

Directions for future research

“We need to find out,” say the authors, “why MAP is more predominant in these patients — whether it’s present because they have RA [rheumatoid arthritis], or whether it caused RA in these patients. If we find that out, then we can target treatment toward the MAP bacteria.”

To this end, the researchers plan to carry out further studies, in the hope that their findings will be replicated.

National studies should now also investigate how many patients get both rheumatoid arthritis and Crohn’s disease, say the scientists. They themselves plan to examine the association further in people from different countries and of different ethnicities.

“Understanding the role of MAP in rheumatoid arthritis,” explains Naser, “means the disease could be treated more effectively. Ultimately, we may be able to administer a combined treatment to target both inflammation and bacterial infection.”

Crohn’s disease: Discovery of two subtypes could lead to better treatments

Crohn’s disease is notoriously difficult to treat due to the course and severity of the disease varying from one case to another. Research by University of North Carolina School of Medicine has discovered two subtypes of the disease – with different gene expressions and clinical features – which may reveal why such variations in disease progression surface between patients.

The discovery of two classes of Crohn’s has implications for scientists to deliver more targeted treatments.

Crohn’s disease – a long-term condition that causes inflammation to the lining of the digestive system – affects almost 1 million people in the United States. While there is no cure for Crohn’s, treatment with anti-inflammatory drugs and immune system suppressors can help improve symptoms.

Around 70 percent of people with Crohn’s will eventually require surgery to remove damaged portions of the digestive tract and reconnect to healthy sections, and as many as 39 percent will require repeated surgery. Surgery may also close fistulas and drain abscesses.

The study findings – published in the journal Gut – build upon existing knowledge of the biology of Crohn’s disease, and they could potentially lead to more effective strategies and personalized treatments to target the debilitating gastrointestinal condition.

“The one-treatment-fits-all approach doesn’t seem to be working for Crohn’s patients,” says co-senior study author Dr. Shehzad Z. Sheikh, Ph.D., assistant professor in University of North Carolina’s (UNC) departments of medicine and genetics.

“It’s plausible that this is because only a subset of patients has the type of disease that responds to standard therapy, whereas, for the rest of the patients, we’re really not hitting the right targets,” he adds.

Genes that varied between subtypes distinguish colon from ileum

With co-senior author Terry Furey, Ph.D., associate professor in UNC’s departments of genetics and biology, Sheikh and team analyzed colon tissue samples that looked healthy and non-inflamed in 21 Crohn’s patients who had undergone surgery. They then mapped levels of gene expression patterns amongst the samples, finding that there were two distinct groups.

“Although we saw a difference between the Crohn’s samples and samples from people without Crohn’s, we saw an even greater difference at the molecular level between these two subsets of the Crohn’s samples – the healthy tissue from Crohn’s patients and the inflamed samples from Crohn’s patients,” says Furey.

Co-first author Jeremy Simon, Ph.D., a research assistant professor in UNC’s department of genetics, notes that how the two disease subtypes differed was surprising.

Despite the samples being colon biopsies, Simon says, many of the genes that were varied between the two Crohn’s subtypes were markers that distinguish the colon from the ileum – the portion of the small intestine that empties into the colon and is usually the first area to be affected by Crohn’s disease.

The pattern of gene expression in one of the disease subtypes resembled healthy colon tissue. However, the gene expression in the second subtype resembled patterns seen in the ileum.

In addition to analyzing gene expression in the sampled tissue, Sheikh and colleagues observed indicators of the epigenetic state of the DNA tissue that can permit or repress nearby gene activity. The team saw a distinction between the two Crohn’s subtypes in the results that suggest the differences in gene expression emerge from variations in the core programming of the affected cells.

Crohn’s subtypes linked to two different clinical illness patterns

The researchers ensured that the fact that the samples were from adults who had undergone surgery did not skew the results, due to treatment and disease histories, by comparing their data to another dataset.

The team examined data from 201 children who had recently been diagnosed with Crohn’s and had not yet been treated. While the tissue samples in the data were from the ileum, the same colon-like and ileum-like disease classes were observed.

“This suggests that these molecular programs or baseline genomic signatures of Crohn’s subtypes exist independently of patients’ ages or treatment histories,” says Sheikh. He also points out that the two signatures are linked to different patterns of clinical illness.

For example, patients with the colon-like subtype were more likely to be characterized by gut inflammation found during colonoscopy, rectal disease, and colon inflammation severe enough to require colon removal.

In future work, Sheikh, Furey, and collaborators aim to develop a diagnostic test for use on tissue or blood samples taken from routine colonoscopies. By identifying which Crohn’s subtype a patient has, healthcare providers can determine the best therapy for treatment.

Scientists find new genetic locations for type 2 diabetes

Scientists from University College London and Imperial College London in the United Kingdom have identified new genetic locations that might make some people more prone to developing type 2 diabetes.

Scientists identify 111 new genetic locations that indicate susceptibility to type 2 diabetes.

Type 2 diabetes affects hundreds of millions of people worldwide, and the numbers have skyrocketed in recent years. According to the World Health Organization (WHO), the number of people with diabetes has almost quadrupledin the past few decades, from 108 million in 1980 to 422 million in 2014.

In the United States, 29 million people currently have diabetes, and 86 million are thought to have prediabetes.

Until now, researchers were aware of 76 chromosomal locations, or “loci,” that underlie this metabolic disease. However, new research analyzed the human genome further and found an additional 111.

The new study – published in the American Journal of Human Genetics – was co-led by Dr. Nikolas Maniatis of University College London’s (UCL) Genetics, Evolution, and Environment department, together with Dr. Toby Andrew of Imperial College London’s Department of Genomics of Common Disease.

Identifying the type 2 diabetes genetic loci

Using a UCL-developed method of genetic mapping, Maniatis and team examined large samples of European and African American people, summarizing 5,800 cases of type 2 diabetes and almost 9,700 healthy controls.

They found that the new loci – together with the ones previously identified – control the expression of more than 266 genes surrounding the genetic location of the disease.

Most of the newly discovered loci were found outside of the coding regions of these genes, but within so-called hotspots that change the expression of these genes in body fat.

Of the newly identified 111 loci, 93 (or 84 percent) were found in both European and African American population samples.

After identifying genetic loci, the next step was to use deep sequence analysis to try to determine the genetic mutations responsible for the disease.

Gene mapping finds areas associated with diabetes-causing genetic loci

Maniatis and colleagues used deep sequencing to further examine three of the cross-population loci with the aim of identifying the genetic mutations. They then investigated a different sample of 94 Europeans with type 2 diabetes, as well as 94 healthy controls.

The researches found that the three loci coincided with chromosomal regions that regulate gene expression, contain epigenetic markers, and present genetic mutations that have been suggested to cause type 2 diabetes.

Dr. Winston Lau, of UCL’s Genetics, Evolution, and Environment department, explains the significance of these findings:

“Our results mean that we can now target the remaining loci on the genetic maps with deep sequencing to try and find the causal mutations within them. We are also very excited that most of the identified disease loci appear to confer risk of disease in diverse populations such as African Americans, implying our findings are likely to be universally applicable and not just confined to Europeans.”

Dr. Maniatis also highlights the contribution their study brings to the research community:

“No disease with a genetic predisposition has been more intensely investigated than type 2 diabetes. We have proven the benefits of gene mapping to identify hundreds of locations where causal mutations might be across many populations, including African Americans. This provides a larger number of characterized loci for scientists to study and will allow us to build a more detailed picture of the genetic architecture of type 2 diabetes,” says the lead author.

Dr. Andrew also adds, “Before we can conduct the functional studies required in order to better understand the molecular basis of this disease, we first need to identify as many plausible candidate loci as possible. Genetic maps are key to this task, by integrating the cross-platform genomic data in a biologically meaningful way.”

What causes pimples?

A pimple is a small pustule or papule. Pimples develop when sebaceous glands, or oil glands, become clogged and infected, leading to swollen, red lesions filled with pus.

Also known as spots or zits, pimples are a part of acne. They are most likely to occur around puberty, but they can happen at any age.

During puberty, hormone production changes. This can cause the sebaceous glands, located at the base of hair follicles, to become overactive. As a result, pimples are most likely to occur during the teenage years and around menstruation, for women.

Pimples most often affect the face, back, chest, and shoulders. This is because there are many sebaceous glands in these areas of skin.

Acne vulgaris, the main cause of pimples, affects over 80 percent of teenagers. After the age of 25 years, it affects 3 percent of men and 12 percent of women.

Here are some key points about pimples. More detail is in the main article.

• • Pimples range in severity, from blackheads to cysts.
  • They happen when the sebaceous glands become more active, dead skin cells clog the pores, and sometimes an infection develops.
  • Pimples often occur in adolescence, but they can affect people at any age.
  • There is not enough evidence to confirm that any particular food causes acne, but following a healthful diet may reduce the risk.

Types

Blackheads, whiteheads, and cysts are all kinds of pimples, but what makes them break out?

There are several different types of pimples, and they have different signs and symptoms:

Whiteheads: Also known as a closed comedo, these are small pimples that remain under the skin. They appear as a small, flesh-colored papule.

Blackheads: Also known as an open comedo, these are clearly visible on the surface of the skin. They are black or dark brown, due to the oxidation of melanin, the skin’s pigment.

Some people mistakenly believe they are caused by dirt, because of their color, and scrub their faces vigorously. Scrubbing does not help. It may irritate the skin and cause other problems.

Papules: These are small, solid, rounded bumps that rise from the skin. They are often pink.

Pustules: These are pimples full of pus. They are clearly visible on the surface of the skin. The base is red and the pus is on the top.

Nodules: These have a similar structure to papules, but they are larger. They can be painful and are embedded deep in the skin.

Cysts: These are clearly visible on the surface of the skin. They are filled with pus and are usually painful. Cysts commonly cause scars.

Why do pimples happen?

Pimples happen when pores become clogged with sebum and dead skin. Sometimes this leads to infection and inflammation. Why they affect some people more than others is largely unknown.

The sebaceous glands and pimples

The sebaceous glands are tiny skin glands that secrete sebum, a waxy or oily substance that lubricates the skin and hair.

Sebaceous glands are found inside the pores of our skin, all over the body, except the palms of the hands and soles of the feet. There are more sebaceous glands on the face and scalp than elsewhere.

As the glands produce sebum inside the pores, new skin cells are constantly growing, and the outer layers of skin are being shed.

Sometimes, dead skin cells are not shed. They remain in the pores and get stuck together by the sticky sebum, causing a blockage in the pore.

Pore blockage is more likely to occur during puberty, as the sebaceous glands produce more sebum at this time.

Bacterial infection

Where sebum and dead skin cells accumulate and block a pore, this encourages the growth of undesirable bacteria, including Propionibacterium acnes (P. acnes), a slow-growing bacterium linked to acne.

Propionibacterium acnes exists harmlessly on our skin, but when the conditions are right, it can reproduce more rapidly and become a problem. The slow-growing bacterium feeds off the sebum and produces a substance that causes an immune response. This leads to skin inflammation and spots.

Although pimples are related to bacterial infection, they are not contagious. One person cannot catch pimples from another.

Risk factors

It is unclear exactly why some people are more prone to pimples than others. Hormone fluctuation and genetic factors may play a role, as acne often runs in families, but some other factors are possible.

Good and bad bacteria

Gentle washing may help prevent infection, but scrubbing can make pimples worse.

Just as in the gut, we have “good” bacteria that protect against disease and “bad” bacteria that cause disease, scientists have suggested that the same may be true for the skin.

Researchers at the Washington University School of Medicine identified two unique strains of P. acnes in the skin of 20 percent of people with pimples, while those with healthy skin tended not to harbor these strains. source

Another strain of P. acnes had the opposite effect. People with pimples tended not to have this strain, but those with healthy skin did have it.

This may indicate that particular types of bacteria determine the severity and frequency of pimples. The researchers suggest that these bacteria may also interact with different factors, such as hormone and sebum levels. They call for more research.

Yeast infections

Acne-type breakouts have also been linked to yeast infections.

Pityrosporum, also known as malassezia or folliculutis, happens when a pityrosporum yeast enters the hair follicles and multiplies, triggering an itchy eruption of tiny, itchy, rounded pimples, that resembles acne. It mainly occurs on the upper chest, shoulders, and upper back, but it can also affect the face.

Most people have this yeast on their skin, but if too much develops, it can cause a problem. It can happen to both men and women in young to middle-age.

Humid, sweaty environments, clothes made of synthetic fibers, and the use of oily skin products can all make this worse.

The condition is common in adolescents, probably because of increased sebaceous gland activity. It is not the same as acne, but it is often confused with it.

Antibiotics that are usually used for acne can make also make the condition worse, as they suppress the bacteria that would otherwise control the yeast. Antifungal treatment is needed in the case of malassezia.

Testosterone sensitivity

Researchers have found a link between acne pimples and higher levels of testosterone and other androgens, the “male” hormones that also exist in lower levels in females.

Higher testosterone levels appear to to trigger greater activity in the sebaceous glands, resulting in more clogged pores and higher chance of acne.

Dietary factors

The role of diet in acne is unclear, but, since a healthy, balanced, diet is known to promote good health, some dietary factors may affect the likelihood of getting acne or pimples.

Vitamins A, D, and E are all known to play a role in maintaining healthy skin, so it is possible that an adequate supply of these vitamins may help prevent acne.

Milk consumption has been associated with acne. If milk does play a role, this could be due to the hormones in milk. However, findings have been inconclusive.

It has often been said that sugar and chocolate trigger acne, but research findings have not supported this.

Studies have linked a low glycemic-index (GI) diet with lower levels of insulin in the blood, lower levels of androgen, and a reduced likelihood of acne.

However, the results are not conclusive. Moreover, advocating a low GI diet could discourage people from consuming enough whole grains and other healthful foods that could provide useful nutrients.

Although acne is related to sebum production, avoiding all fat in the diet is not advisable. Healthy polyunsaturated and monounsaturated fats are necessary for key bodily functions. A fat-free or very low-fat diet can cause the skin to dry out and prompt the body to increase sebum production.

A good intake of fats from nuts, seeds, and olive oil may help by keeping inflammation in check, supporting the body in maintaining healthy blood sugar levels, and maintaining good skin moisture levels so as to provide an effective barrier and immune response to prevent bacterial infection.

According to the American Academy of Dermatology (AAD), “There is not enough data to recommend dietary changes for acne patients.”

If dietary changes are to play a role in acne treatment, the AAD suggest that this should be as a “complement to proven acne treatments,” rather than as a sole treatment. They suggest that individuals monitor themselves to see what might trigger a breakout.

Tips include:

• keeping a food diary, and sharing it with a dermatologist
• waiting for 12 weeks after cutting out a particular food, as it may take time to see the impact
• continuing with regular acne treatment while making any dietary changes

Some medical conditions also increase the chance of pimples, for example, polycystic ovarian syndrome (PCOS).

Since acne appears to stem from a complex interaction of nutrients, hormones, and other factors, it is difficult to pinpoint exactly what causes pimples to worsen.