The exact mechanism of action of Latisse is not clearly understood but it appears to be a prostaglandin receptor binder . Prostaglandin receptors are present in here and is thought that prostaglandin receptors are somehow involved in the development and regrowth of hair follicles.

Latisse® is a prescription only product that is designed to be applied once daily to the base of the upper eyelashes with a single use a sterile applicator. Despite the intention to make Latisse® prescription only,  much like other drugs for which patients might wish to use but don’t want to get a prescription to see a physician about Latisse® is widely available online without direct physician supervision. This is unfortunate because the teeth can have very annoying and potentially permanent side effects. These include a plum shade discoloration of the eyelid, macular edema which can be very serious even lead to blindness, a condition called punctate epithelial keratitis which can lead to significant itching and irritation of the eyes, as well as dry eye, eyelid swelling and injection of the conjunctival blood vessels making the eye seem reddish or pink. In addition though not mentioned in the product insert there are reports of Latisse® leading to darkening of the iris.

Although Latisse is a prescription only product it’s very easy to purchase this drug online without a prescription. The top of the Google search list for pilot case online is a site where you simply submit a medical form history and a “patient marks licensed physician will carefully ensure Latisse is a safe  option free you to use before we send your order.” They even advertise a discount for Valentine’s Day few by two more bottles. The retail price@drugstore.com for one bottle for peace is $115.99, but several online sources appear to be selling Latisse for between $70 and $85 per bottle. A bottle will last one month if applied as directed to both upper lids and even the manufacturer notes that Latisse only works as long as you continue to use it. Whether longer thicker eyelashes are worth approximately hundred dollars a month plus the risk of serious side disorders that could even affect vision and cosmetic or annoying eyelid problems is for each individual to decide.

Resource: Latisse side effects

Let’s look at the evidence for transmission of the various STDs by oral-genital contact.

HIV:  Human Immunodeficiency Virus, the cause of AIDS, is the STD many fear most.  It can be transmitted when a body fluid containing the virus gains access to another person’s mucous membranes or bloodstream.   Unquestionably HIV is transmitted by anal and vaginal intercourse.  There are at least a few cases where it is believed that the HIV virus was transmitted to the receptive partner after oral sex with ejaculation.  Oral sex without ejaculation into the mouth is theoretically possible, but is felt to be extraordinarily unlikely. The risk of contracting HIV from a single incidence of anal intercourse with with ejaculation and no condom use with an HIV infected male has been estimated at 1:100.  Extensive study has been done in trying to find out what the incidence of contracting HIV from oral sex with ejaculation with an HIV infected male, but these studies all have confounding variables.  The real problem is that all of these studies have been in gay male populations, and a low percentage of the men had only oral sex.   On second and subsequent interviews many times the history changed, and made other routes of transmission more likely.  In one study it was estimated that there were zero cases of conversion in a population after over 35,000 incidences of oral sex.  All said, although it is possible to contact HIV from oral sex, the chances are very low. Low enough that if oral sex is a behavior that replaces anal intercourse in gay men the benefit of avoiding the high risk behavior likely greatly outweighs the risks of oral sex in this situation.

Herpes Simplex:  This may be the most common STD transmitted by oral sex.  Up to 70% of teens are estimate d to have been infected with the herpes simplex 1 virus, the cause of >90% of oral herpes cases.  Many others, and many of the same people also have been infected with the herpes simplex 2 virus, the cause of >90% of genital herpes.  The problem with herpes simplex is that despite popular belief, an infected person can shed the herpes virus at times when they have no symptoms or visible evidence of infection. It is believed to be  fairly common to transmit the herpes simplex virus either from the mouth to the genitalia, or from the genitalia to the mouth during oral sex.  The incidence of HSV transmission by oral sex is not well studied.

Gonorrhea:  Gonorrhea, caused by the bacteria Nisseria gonococcus, is an STD that typically causes painful urination and  a discharge of pus from the urethra in men.  In women it can be asymptomatic, can cause a vaginal or cervical discharge, or can cause more serious infection of the fallopian tubes and or ovaries, called Pelvic Inflammatory Disease (PID).  Gonorrhea can also infect the throat or tonsils.  The route of this infection appears to be oral sex, generally receptive oral sex with the penis in the mouth.  It is less clear whether cunnilingus can transmit gonorrhea although it is felt that this is very rare if it ever happens.  Men likely only contact gonococcus from vaginal or anal intercourse or from an infected partner during receptive oral sex.

Chlamydia:  There is less data about transmission of Chlamydia by oral sex.  It is generally felt to be possible to transmit Chlamydia both as the person performing and the person receiving fellatio.  The incidence of this is just not known.

Syphilis:  Syphilis is fairly uncommon in the US, but transmission of syphilis during oral sex is relatively easy, and is felt to be a relatively common cause of transmission, possibly up to 15% of cases in some areas of the US.

HPV:  HPV is probably the most prevalent STD in the world today. The HPV virus can be transmitted to the throat or mouth during oral sex.  The incidence of this is poorly understood, but there is an increasing rate of HPV positive head and neck cancers in the last 30 years.  Many experts feel that this correlates to increasing acceptance of oral sex.  Oral cancer has historically been primarily a disease of older adults with a long history of smoking and drinking, or in younger persons who use oral tobacco.  In recent years the incidence in younger non-tobacco users has increased, and many of these cancers are HPV positive on testing.

Hepatitis:  There is debate whether hepatitis B can be transmitted by oral sex, but if possible it is felt to be very unlikely.   Hepatitis A can clearly be transmitted by oral-anal sex, and is much more common in the gay male population than in the heterosexual population.

In summary oral sex is not safe sex, but it is far less risky than either vaginal or anal intercourse regarding STD transmission.  In addition the risk of pregnancy in heterosexual oral sex is near zero.   Avoiding receiving ejaculate in the mouth greatly lowers the risk of transmission of HIV, though probably not the risk of herpes, gonorrhea, or HPV.  Condom use for men, or use of a dental dam in women seems effective in markedly reducing the risk of most STDs with oral sex, but may not be common practice.

Psychological Issues:  Oral sex is clearly an intimate act.  Most psychologists agree that sex, either oral sex or sexual intercourse, brings a relationship to a different level.  How this type of intimacy affects a relationship, the self esteem of the participants, and future feelings about relationships and intimacy are subjects worthy of consideration, but I know of no research into this topic.

So, “How safe is oral sex?”  What do you want to tell your children about oral sex as a part of their sex education? You can decide now based on the discussion above and whether it involves men having sex with other men (MSM)  vs. heterosexual oral sex.  One risk of labeling oral sex a high-risk behavior in MSM is that it may leave gay men feeling that its risk is equal to anal intercourse, which is far from the truth.  If oral sex is an alternative to anal intercourse for MSM then it greatly reduces the risk of HIV transmission.

Add Some Red to Black Friday and I’ll give some Green to the American Cancer Society

Millions of Americans shop for Christmas gift bargains on Black Friday every year.  I encourage you to give a gift on Black Friday that costs you nothing more that a little time, and which can help you feel you have truly given life and hope during this holiday season.

My readers will know that I’m a big proponent of regular blood donations.  Kay, my wife has ovarian cancer and has been a recipient of donated blood when her blood counts get low from chemotherapy.  Cancer patients are among the highest users of donated blood products from red blood cells to platelets.  I’m donating regularly to be sure our family puts more blood into the blood banking system than we take out. I want you to join with me on the Friday after Thanksgiving this year by paying a visit to your local blood donation center.  There are even potential blood donation health benefits.

I’m putting out a challenge to readers, your friends and anyone else you can contact.  Black Friday is a day when many of us are out and about shopping and getting ready for the holidays.  The holiday season is also a time when blood donations tend to fall behind need.  Here is the challenge:

I’ll donate $1. (up to $1000) for every comment to this post or tweet me @DoctorPullen telling me that you have or intend to go to your local blood donation center on Black Friday and donate blood. $1. may sound like chump change, but I want to get 1000+ people who would otherwise not donate blood to do so this Friday.  We are in a world of easy communication, and I bet everyone who reads this knows 10 people who are in a position to get to their blood donation center this black Friday and donate.  Just do it!

Take a break from shopping, get off your feet, and relax while you give one special holiday gift.  Use the twitter or facebook links to send this off to your friends, tell your coworkers, shout from the roof tops, whatever but let’s make this Black Friday blood red with our generosity.

My daughter, son and I plan to go to the local Cascade Regional Blood Bank center in Puyallup Friday. I checked and they are open 7:30 AM – 5:00PM.  I’ll try to keep a counter going on the site to let you all know how we are doing.

They Turned Me Away Today

Egg on my face.  I went today to donate, but was turned away because I went to Belize on vacation a couple of months age, an area with malaria exposure potential.  I’m now ineligible for a year, joining a majority of the rest of Americans.  If you are among the 37% who are eligible donors get to your blood donation center and give.  Keep our blood supply safe and plentiful.  Happy Thanksgiving.

Hormonal acne has always been among the more difficult types of acne to treat, and in recent years the use of spironolactone for its anti-androgen effects has been found to be helpful for this particular type of acne.  When a woman’s acne is much worse in the week or two prior to her menses or around the time of menopause oftentimes the acne will respond to the anti-androgen effects of spironolactone.  The usual dose is 50-100 mg twice daily.  In adolescents and young women the combination of low-androgenic oral contraceptives is sometimes more effective than spironolactone alone.

The use of spironolactone for suppression of androgenic hair growth by women is also widespread.  Spironolactone can be effective in suppression of facial hair and to a lesser degree body hair.  Again the dose often used is 50-100 mg twice daily.  Polycystic ovarian disease is one of the common medical problems where spironolactone is used for suppression of facial hair growth.

On the other side of hair growth, spironolactone is being used without much evidence to support its efficacy in men with male pattern baldness.   Topical preparations are proported to be helpful for this indication, although I have to say I’m skeptical and the evidence looks pretty sketchy.  Some advocates suggest that adding spironolactone topically to systemic finasteride (Propecia) gives additive anti-androgenic effects at preventing male pattern baldness hair loss.

PMS is a  less well documented and popular use of spironolactone.  Some women find that the drug lessens the severity of the premenstrual dysphoric and fluid retention symptoms.  The primary effect of spironolactone is inhibition of the adrenal hormone aldosterone.  Aldosterone leads to elevation of blood pressure, so inhibition of aldosterone can cause dieresis and so lessen the PMS symptoms of bloating, fluid retention, and premenstrual weight gain.  It is unclear whether the anti-estrogen effects of spironolactone play a role in reducing the emotional symptoms of PMS, or whether any benefit in this regard is related to the diuretic effects.

Traditional uses of spironolactone are more mundane but well documented.  Likely the most common FDA approved uses of spironolactone are to spare potassium loss in combination with a thiazide diuretic, in such fixed dose drugs as Aldactazide and for treatment of congestive heart failure in patients. A commonly noted NEJM article showed that in patients with serious heart failure, LV ejection fraction less than 35%, usually also on and ACE or ARB and loop diuretic like furosemide patients on spironolactone had significantly lower death rates than the control group on placebo.  For more information about furosemide please visit furosemide side effects for a nice resource online.  Other typical diuretic uses of spironolactone are patients with ascites due to cirrhosis of the liver.  The theory behind this is that effects of aldosterone may be harmful to the myocardial cell function.

Spironolactone has potential side effects that can bother patients, and can lead to drug interaction issues.  Common side effects of spironolactone include elevation of serum potassium levels that can be severe at times, Gynecomastia, and diarrhea.  Serious drug interaction side effects can occur with numerous medications, but of special mention are additive potassium elevation effects when used with angiotensin receptor blockers or angiotensin converting enzyme inhibitors, with various other antihypertensive or other cardiac medications.

Spironolactone is pregnancy category D, and carries a black box warning that long term use in rats has been associated with tumor growth and toxicity.

It will be interesting to see if use of the aromatase inhibitors for estrogen sensitive conditions other than breast and ovarian cancer becomes more widespread in future years.  Their difficult side effects of the aromatase inhibitors makes this less likely than if they were easy to tolerate.

Like many new drugs on the market Lysteda is not really new. It has been used for years as an IV drug for prevention of bleeding in hemophilia patients for dental extraction and other surgical procedures.  Tranexamic acid works as a competitive inhibitor of plasmin at one of its receptors on the fibrin matrix.  By inhibiting plamin function the clotting of blood that involves the production of fibrin is stabilized, and bleeding during menses is diminished.  In two trials menstrual bleeding by women was reduced by about 38-39% as compared to 13% reduction by placebo.

The major side effects of Lysteda are related to its mechanism of action and include increased risk of blood clots in the form of veinous thromboembolism in the legs as DVT, and of stroke and heart attacks.  Use in combination with oral contraceptives significantly increases the risk of thromboembolic adverse events and is recommended only in extreme circumstances. Frankly I cannot imagine what this situation would be, as there are alternatives to Lysteda in this situation.  Lysteda is also cautioned in women at higher risk of DVT, including smokers over the age of 35 and obese smokers.  Another serious thromboembloic side effect that has been reported with Lysteda is retinal vein and retinal artery occlusion.  These can cause loss of vision, and any visual symptoms while on Lysteda need immediate opthalmologic attention.

Less serious Lysteda side effects include headache, nasal symptoms, backache, abdominal pain, migraine, anemia, and various musculskeletal pains and arthralgias.  Overall the tolerability in patients using Lysteda seemed fairly good in the published clinical trials.  Most of the serious side effects noted above have been reported in after-market experience and although uncommon are serious enough to make Lysteda a drug physicians tend to use only in very select circumstances.

After studying the advantages and risks or Lysteda I think the niche I’ll consider use of Lysteda is in the woman at low risk of thromboembolic events who has very heavy menses, for some reason is not controlled by birth control pills or has problems with birth control pills, who has a reason not to use the Mirina IUD, who wants to maintain fertility, and who can afford the relatively high cost of this drug.  See the insured, late teens to late 20’s woman who gets side effects of birth control pills and plans more children yet has extremely heavy menses.  Keep in mind that Lysteda is only for heavy menses, and does not treat other PMS symptoms, does not provide contraception, does not protect against STDs, and only reduces menstrual bleeding by less than 50%.  Compare this with the alternatives:

Overall the niche for Lysteda is small, but it is one more fairly recent addition to our war chest of tools to treat a sometimes very challenging problem that can cause considerable morbidity for affected women.

This is nice to have as an option given the significant morbidity women experience from menorrhagia.  Hysterectomy has been suggested by some as the most cost effective treatment of menorrhagia.  Endometrial ablation is very popular today among women who percieve hysterectomy as too agressive for their preferences.  Lysteda is among the options, especially for women who want to preserve their fertility and who are at low risk for coagulation problems.

Laughing gas, or nitrous oxide seems to be rising in popularity for use in labor for pain control.  It has been a mainstay of dental anesthesia for years, and is used as a part of conscious sedation in many hospital and some office settings.  My concern is that the effects of nitrous oxide on the fetus have really not been studied.  It’s probably safe, but is probably good enough?  Check out this article.  The advocates seem to be strongly in favor of the use of nitrous for labor, but their argument seems more a business argument than a medical one.  What I read is, “Get Laughing Gas for Your Birthing Center” and have a heads up on the competition for patients.

Here are a couple of quotes from the MedPage article:

Another possible hang-up is concern over safety.

There’s been no investigation into the effects of in utero exposure to nitrous oxide, and nitrous oxide exposure to allied health professionals often exceeds federal occupational safety limits, Palmer cautioned.

Here is a back and forth banter. Susanne Serat is a nurse practitioner midwife in New Hampshire who has been using nitrous oxide for her patients.  Craig Palmer is chair of the obstetric anesthesia department at the University of Arizona.

Dartmouth may wait to make its final decision on instituting nitrous oxide during labor until they see Vanderbilt’s data and have more safety assurance in hand, Serat noted.

But that would be a mistake, Rooks argued, noting it will be years before that data comes in, whereas the European experience shows millions of women having used it without any evidence of problems.

“Just because people have been using it doesn’t mean we know enough about its safety,” Palmer countered.

It took a long time for epidurals to be accepted as safe, too, noted Rooks.

“Like anything it will come slowly,” she predicted.

But grassroots acceptance is being helped along by women like Jaeger, who has been

Check out the full article at:  Laughing Gas Bringing Smiles to More Women in Labor

By Crystal Phend, Senior Staff Writer, MedPage Today
Published: April 27, 2011

Iron Deficiency Anemia Blood Smear

Microcytic anemia is among the most common problems seen in the family physician’s office.   If you are a young woman or child with anemia, most likely it’s microcytic anemia due to iron deficiency.  I often see patients who just assume that anemia means iron deficiency.

When a physician sees a patient with anemia the first thing they look at is the size of the red blood cells.  Microcytic denotes that the size of the red blood cells is smaller than normal red blood cells, and anemia is the name given to a reduced red blood cell hemoglobin concentration in the blood.  The size of the red blood cells is measured as the mean corpuscular volume (MCV) and is normally between 80-100 microns.  When the MCV is less than 80 a patient is said to have microcytosis, and when it’s > 100 they are said to have macrocytosis.  Microcytic anemia is when the hemoglobin concentration (Hgb) is <12 in women or <13 in men, and the MCV is <80.  For more information blood counts see a prior post Complete Blood Count (CBC).

Iron deficiency is by far the most common cause of microcytic anemia.  When a patient is found to have a microcytic anemia on a CBC the evaluation usually begins with an assessment of the patient’s iron status, a reticulocyte (newly produced red blood cell) count to assess the percentage of the red blood cells that are newly produced, and an assessment of why the patient is iron deficient.  If iron deficiency is confirmed next we try to find the cause of the iron deficiency.  Finding the cause of the blood loss may be simple, as in women with excessive menstrual blood loss or patients where there is a clear history of intestinal bleeding.  When it is not obvious, testing for occult blood loss in the stool is needed. Treatment of iron deficiency consists of stopping  the blood loss if possible by treatment of the cause, and replacement of the iron supplies.  This can usually be done with oral iron, but occasionally patients either do not absorb adequate iron from the GI tract or cannot tolerate the side effects of oral iron.  Constipation and abdominal pain are common side effects of oral iron supplementation.   In cases where iron deficiency is refractory to oral iron, iron can be infused IV.  There are risks of severe allergic reactions, even shock and death with IV iron, and this is done only when absolutely needed. Other fairly common causes of microcytic anemia include:

• Thallasemia minor:  a genetic mutation of the hemoglobin molecule that causes very small red blood cells (MCV typically 60-70) and low normal hemoglobin concentrations or mild anemia.  This is usually an easy diagnosis when the patient is asymptomatic, has normal iron levels, and a very low MCV.
• Lead poisoning needs to be suspected in children with possible lead paint exposure, adults with occupational or recreational exposure (battery workers, ammunition reloaders). It can be confirmed with serum lead testing.
• Other hereditary conditions like hereditary spherocytosis or hereditary eliptocytosis.  These are due to genetic mutations in red blood cell wall proteins that can lead to very small red blood cells that have fragile cell membranes.  Testing for red blood cell fragility can confirm the diagnosis.
• Anemia of chronic disease is typically a normocytic anemia, although it is sometimes microcytic.  This is when due to a chronic illness, most commonly renal disease, but sometimes general poor health, the bone marrow under produces red blood cells.

Other causes of microcytic anemia are quite uncommon, and if none of the above diagnoses is made, bone marrow aspiration or biopsy and specialty consultation with a hematologist may be needed for evaluation. Overall most patients with microcytic anemia have benign causes and good response to treatment with iron supplementation, but it is key in iron deficiency to figure out the cause of the iron deficiency.  If the anemia does not respond to iron therapy to figure out if the iron is not absorbed, the patient is not taking the iron (non-compliance), or if there is a cause other than iron deficiency.  Iron deficiency is so common that in a low risk patient, like a teenage girl with heavy menses, it may be appropriate just to give iron supplementation and get a follow up hemoglobin level without further assessment. In adults, especially adults over age 35-40, it’s key to assess for GI blood loss, and if present to evaluate the colon for polyps or cancer and if not found to consider upper GI sources of blood loss like peptic ulcer or gastritis.

It’s interesting that the USPSTF is publishing new guidelines for screening of osteoporosis just as more questions develop about the long term treatment of osteoporosis with bisphosphonates.  In the first USPSTF recommendation update that’s been released after the new protocol for posting anticipated updates for public comment, the task force now gives a Grade B recommendation for osteoporosis screening for all women age 65 or older, as well as for younger women who are estimated to have a risk as high or higher than  a 65 year old woman with no additional risk factors.

The statement specifically recommends DEXA screening of the hip and lumbar spine, but and even recommends a tool to use to assess risk in younger women called the FRAX Risk Assessment Tool.

No recommendation (Grade I: insufficient evidence) is given to screening for men.

There has been a lot written about the risks of atypical femur fractures and osteonecrosis of the jaw in long term treatment with bisphosphonates.  The benefits of these drugs seems to outweigh these risks in general.  Still it is not clear how long we should use these drugs, and whether the benefits are lasting after a several year course of treatment, or only last as long as treatment continues.  Clearly there is more research needed to answer these questions.

The task force also gives no specific guidelines as to how to assess the risk for women age less than 65.  Generally considered risk factors for osteoporosis include smoking, thyroid therapy, corticosteroid treatment, thin body habitus, poor calcium intake, sedentary lifestyle, and prior fractures.

My practice has been to try to screen women in the 50-65 age range if they have multiple risk factors or at 65 if not.  I’ll continue this routine, but it’s good to have the new recommendation as it will make Medicare coverage for DEXA a preventative service, I believe with no co-pay or deductible.  Comments as to experience with this issue are welcome on this medical blog.

Physicians talk of the lipid profile, or lipid type while most patients want to know about their cholesterol.  We really are on the same team, looking for the same goals of reducing the risk of heart and artery disease caused by abnormally levels of the types of lipids that lead to atherosclerosis.  We just have different words we use.  The jargon physicians use can be confusion, and lipid type is a good example.  First some definitions:

Lipid: really another word for fat.  A lipid is a substance that disolves in alchohol but not in water.  Examples of lipids are wax, oil and other fats.

Cholesterol: a specific lipid that is used for many purposes in the body including cell membranes, hormones, vitamin D production and bile production.  It consists of a sterol carbohydrate ring with specific side chains.

Lipoprotein: a particle manufactured in the liver that consists of lipids and protein that circulates in the bloodstream.

Triglyceride: molecule made up of a three carbon molecule glycerin with three long carbon chain fatty acids attached, i.e. “tri” for three + glyceride. Practically these are the fatty particles in the blood stream that did not get packaged into lipoproteins in the first pass of the blood from the gut through the liver.

HDL cholesterol: (High density lipoprotein) Think good cholesterol here.  The HDL  lipoprotein particle consists of more proteins which are more dense, and less lipids which are less dense, so the lipoprotein is high in density.  There are several subsets of HDL, but in general a high HDL level is good.  HDL cholesterol functions in part to remove cholesterol from places it does not belong and return it to the liver to be repackaged and better used.

LDL cholesterol: (Low density lipoprotein) Think bad cholesterol here.  A lipoprotein that is higher in lipid and lower in protein making it low density.  In general high levels of LDL cholesterol are not good, as they increase the risk of atherosclerosis and heart disease.  LDL cholesterol is the primary vehicle for carrying cholesterol in the blood stream.  When present in large amounts cholesterol is often put where it can cause harm, like on the lining of blood vessels.

CRP: (C-reactive protein or hsCPR for highly sensitive CRP) is a marker of inflammation, and is used sometimes to assess risk of heart disease when the cardiovascular risk based on the rest of the lipid measurements and the other risk factors do not lead to a clear decision on lipid management.

Non-HDL cholesterol: This is simply calculated by subtracting the HDL cholesterol level from the total cholesterol level.  non-HCL cholesterol is a secondary target for treating lipids, after the LDL goal is met.

Direct LDL: usually the LDL level is calculated using the formula:

Total Cholesterol – HDL cholesterol – Triglycerides/5 = LDL cholesterol

This formula is quite accurate except when the triglyceride level is over 400-500.  High triglyceride levels make this calculation less accurate, so in those cases a more expensive test is used to measure the LDL cholesterol directly.

Physicians use these numbers along with a patients other risk factors to decide on whether to treat them with medication for abnormal lipid measurements.  In general the more risk factors for heart disease a patient has the more likely they are to warrant medication treatment.

The risk factors recommended by the National Institute of Health (through the NHBLI)  for this decision making include:

Table 3. Major Risk Factors (Exclusive of LDL Cholesterol) That Modify LDL Goals*

- Cigarette smoking

- Hypertension (BP ³140/90 mmHg or on antihypertensive medication)

-Low HDL cholesterol (<40 mg/dL)†

-Family history of premature CHD (CHD in male first degree relative <55 years; CHD in female first degree relative <65 years)

-Age (men ³45 years; women ³55 years)*

* In ATP III, diabetes is regarded as a CHD risk equivalent.

† HDL cholesterol ³60

(table from the NIH site)

The levels of cholesterol are broken down into categories:

Table 2. ATP III Classification of LDL, Total, and HDL Cholesterol (mg/dL)

LDL Cholesterol

<100                                       Optimal

100-129                                 Near optimal/above optimal

130-159                                 Borderline high

160-189                                 High

>190                                       Very high

Total Cholesterol

<200                                Desirable

200-239                          Borderline high

³240                                  High

HDL Cholesterol

<40                                    Low

>60                                     High

(table from the NIH site)

The recommendations for goal LDL cholesterol are as follows:

Three Categories of Risk that Modify LDL Cholesterol Goals

Risk Category LDL Goal (mg/dL)

CHD and CHD risk equivalents           <100

Multiple (2+) risk factors*                   <130

Zero to one risk factor                           <160

* Risk factors that modify the LDL goal are listed in Table 3

(from the NIH site)

Using these recommendations a woman age 67 who does not smoke, has a BP < 140/90 on no blood pressure medication, has an HDL cholesterol of 38, and has no coronary heart disease in her mother, father, or siblings would have 2 risk factors (age plus low HDL cholesterol) making her goal LDL <130.

Similarly a man age 40 who smokes, is on BP medication, and whose father had his first heart attack at age 50 with an HDL of 33 would have three risk factors (smoking, blood pressure and family history)  so his goal LDL cholesterol would be <130 unless his Framingham calculated risk of developing Coronary disease in the next 10 years is >20%.

Here is a link to the calculator provided by the NIH  to calculate Framingham Risk:

Framingham Risk Calculator

Using this calculator the 10 year risk of the man above would be 22% if his current systolic BP was 130 on medication, so he falls into the CHD equivalent category and has a goal of <100 for LDL cholesterol.

Treating LDL cholesterol is usually pretty straightforward.  We try to get patients to eat a diet low in total fat and saturated fat (primarily animal fat) to avoid trans fatty acids, and to lose weight.  If this is not adequate we usually add a medication in the statin family.  Many generic statins are available and can keep costs of treatment fairly low, and most patients tolerate statins well.  Some patients do not and red yeast rice is sometimes tolerated by those patients.  It has a statin-like effect.  Statins can lower LDL cholesterol by 25-55% in most patients.  If statins are not tolerated, or if you are a woman who may become pregnant (absolute contraindication to statins) then other medications are sometimes used.

Treating low HDL cholesterol is more difficult, and often slow release niacin is used for this purpose, but it is sometimes difficult to tolerate because of flushing and itching side effects.

Treating triglycerides is important if they are extremely high.  Levels >500 can put you at risk for pancreatitis, and need to be treated.  Levels between 150 and 500 are suboptimal, and are sometimes treated.

In general the goals for non-HCL cholesterol are the LDL goals + 30.

Hopefully this has been helpful in understanding your lipid profile.  If you have suggestions for improvement, or other comments, please leave them in the comments section below.

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Other articles you may enjoy:

Diabetes Mamagement: It’s Not All About Blood Sugars

Blood Pressure Control: No Excuses. Just Do It!

Personality: How it Affects Your Diet

October 20, 2010, 12:01 am

Do Women Sweat Differently Than Men?

The PARP drugs so far have been well tolerated and seem to have few serious side effects.  Cheers to out to our bench scientists doing basic science for discovering these DNA repair pathways, and taking that knowledge and using it to develop yet another promising class of drugs.  I have a vested interest in these trials as my wife has a BRCA2 gene mutation and is getting treatment for advanced ovarian cancer, so stay tuned for any further advances in studies on these new drugs.

VBAC and home birth: evaluating the evidence

Thanks to a recent pronouncement from the American College of Obstetricians and Gynecologists, my two-year old daughter, who arrived via a vaginal birth after Cesarean section (VBAC), may not be a medical rarity for much longer. In a previous post, I discussed possible causes for the steep 15-year decline in the percentage of U.S. women who have delivered a child vaginally after a previous Cesarean birth (currently fewer than 1 in 10). In March, at a conference held at the National Institues of Health in Bethesda, Maryland, an expert panel concluded that the scientific evidence did not support ACOG’s existing recommendation that surgical and anesthesia personnel be “immediately available” during a trial of labor. However, they found evidence that this restrictive requirement had caused many hospitals without 24-hour availability of these services to discontinue VBAC entirely.

To its credit, last week ACOG released an updated version of the guideline that states that a trial of labor is a reasonable option for the vast majority of women who desire a vaginal delivery after a previous Cesarean, including those who have had more than one prior Cesarean and those carrying twins. While continuing to assert that mothers and babies are best served by access to emergency resources, they add: “Respect for patient autonomy also argues that … [an institutional no-VBAC policy] cannot be used to force women to have cesarean delivery or to deny care to women in labor who decline to have a repeat cesarean delivery.” Amen.

Now I’ll to turn to another controversial maternity care topic: home birth. The subject of a widely viewed 2008 documentary and Time Magazine story, out-of-hospital births represented less than 1 percent of all births in the U.S. in 2005, according to government researchers. A recent meta-analysis of previous studies comparing planned home and planned hospital births that concluded that the former was “associated with a tripling of the neonatal mortality rate” elicited a variety of reactions from health professionals in the U.S. and abroad, ranging from ACOG’s reiterating its opposition to home births to calls for more research by the American College of Nurse Midwives and the UK’s Royal College of Obstetricians and Gynecologists.

I agree that more research is needed. But as for the analysis itself, there are at least two reasons to question whether it should cause many (or any) women to reconsider their home birth plans. First, while “tripling” in neonatal deaths sounds scary, this is a relative rather than an absolute difference in risk. Reading the fine print, neonatal death occurred in 0.15 percent for planned home and 0.04 percent for planned hospital births. That’s an absolute risk difference of just 0.11 percent, or about 1 extra death for every 1000 births. This difference is very close to the small increased risk of neonatal death during attempted VBAC versus repeat Cesarean section (0.8 extra deaths for every 1000 births), which ACOG has acknowledged should be a mother’s choice.

Second, all but 3 of the 12 studies included in the meta-analysis were conducted prior to the year 2000, in populations with much lower Cesarean rates than in the U.S. Overall, only 9.3% of women in the planned hospital birth groups had Cesarean deliveries – a far cry from the 32% that currently occur in the U.S. So while this study’s results are most applicable to countries in other parts of the world that have Cesarean rates of 10% or less, it’s not clear if it captured the maternal complications that invariably result from doing 3 times as many surgeries.

The bottom line? The available evidence indicates that planned home birth is no riskier for babies, compared to planned hospital birth, than is attempting VBAC compared to choosing a repeat Cesarean delivery.

 Originally published Thursday, June 17, 2010

Only YOU can develop your child’s brain!

Child centered parenting is a relatively new phenomenon, made possible by the increased security and increased leisure of contemporary life. Where once it was commonplace to send even young children out to work to contribute to the family’s support, childhood is now acknowledged as a protected space.

The change in philosophy has led to a change in the expectations about mothers. After World War II mothers, who were previously held responsible for raising healthy children with good manners, were also tasked with raising emotionally secure adults. This responsibility was seen as requiring a “child centered” approach, giving pride of place to children’s needs over mothers’ needs.

So far, so good. But in the intervening years, the purported responsibilities of mothering have grown dramatically, notably expressed as a commitment to “intensive mothering” also known as attachment parenting. Among those responsibilities is one entirely new claim, the notion that mothers are not responsible merely for physical health, acculturation and emotional security, but are also responsible for a child’s brain development. Whereas there is copious scientific evidence to support assigning the health and socialization tasks to mothers, there is little to none supporting the notion that mothers exercise substantial control over children’s brain development. No matter. An virtual industry has arisen to promote the idea that only mothers can develop a child’s brain.

Canadian sociologist Glenda Wall details the new responsibility in her paper HYPERLINK “http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6VBD-4YJ14B4-2&_user=10&_coverDate=06%2F30%2F2010&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1370757039&_rerunOrigin=scholar.google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=5b94801a0d125d0dc70be71a733e1ab6″HYPERLINK “http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6VBD-4YJ14B4-2&_user=10&_coverDate=06%2F30%2F2010&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1370757039&_rerunOrigin=scholar.google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=5b94801a0d125d0dc70be71a733e1ab6″Mothers’ experiences with intensive parenting and brain development discourse.

Over the 1990s and into the current decade government agencies, non-profit foundations, and child-rearing experts undertook to educate parents and the public in general about the importance of spending ample, one-on-one quality time with children in order to stimulate brain development and future brain potential…

The claims being made in the advice literature that has resulted, while presented as fact, have been the subject of some scientific debate. Several authors suggest, among other things, that there is in fact little evidence in the field of neurology to support the claim that ‘extra enrichment’ … has any beneficial effect on future intelligence or success.

Despite scientific critiques however, the brain development advice itself borrows from the language and authority of neuroscience to frame children’s brains as technologically complex machines that need the correct inputs in order to attain maximum efficiency at a later time …

Wall explains how this new responsibility has put increased pressure on mothers.

Parents and caregivers are cast as the engineers and programmers charged with the task of making the correct inputs, and the potential consequences of neglecting to give children what they need in this regard are portrayed as dire…

In other words, there are now new ways for mothers to screw up and bring opprobrium down on themselves. Not only are mothers blamed for children’s poor manners and psychological issues, but they are now held to be at fault if their children are not intellectually superior.

Wall’s critique is insightful, not merely because she explores the lack of evidence for our new found belief that mothers are responsible for optimal brain development. Wall also casts light on the cultural assumptions that buttress this belief: the assumption that we exercise far more control over health and development than we actually do, and the assumption that parents should do more than aspire to intellectual and professional success for children, they should consciously plan for it.

In an age of intensive, and child-centered parenting, the imperative for parents to plan for, control, and manage the lives of their children to optimize their future chances … The institutional practices that have grown up around prenatal education and planning, the promises made in the marketing of educational toys, and the promotion of lessons, and various types of cultural enrichment all contribute to a cultural understanding that parents (and especially mothers) have a duty, and the ability, to control and shape the lives of their children to a very fine degree.

These assumptions have profound implications for mothers and children.

The view of childhood embedded in brain development discourse is certainly one of children as highly malleable, as parental projects full of potential, but potential that can only be activated with appropriate and intensive parental inputs. Children’s current happiness is also emphasized less in this discourse than is their future potential for success.. Rather it is desirable only in so far as it contributes to potential success, and coincides with parental behavior that promotes brain development. At the same time childhood intelligence has become elevated as an important virtue (over and above happiness) and manifestations of it are more likely to be seen as evidence of good parenting.

Hence the moralizing and hectoring that is so common among attachment parenting proponents. Everything they champion – breastfeeding, babywearing, etc. – is not merely a choice, but it is supposedly a demonstration of commitment to raising smarter, more successful children. In other words, mothering has become a competition.

The focus on intelligence in brain development discourse is linked to an implicit endorsement of competition in this regard between children and between parents. As Nadesan notes … the brain development turn in the 1990s accelerated a trend in parental desires to have children who exceed the norm intellectually…

Proponents of attachment parenting need to look carefully at the assumptions underlying their philosophy and stop the hectoring and moralizing that seem to flow from their philosophy.

AP proponents assume that they can enhance the neurodevelopment of their own children and disparage mothers who refuse to optimize the neurodevelopment of their children. Yet there is really no evidence that mothers’ choices enhance neurodevelopment and hence no basis to assume that mothers who make different choices don’t care about their child’s intelligence.

AP proponents assume that children in their role as future adults are in competition with one another and that mothers should strive to give their children competitive advantages. They also assume that parents are in competition with each other and that a child’s achievements are weapons in that competition. The parent with the smartest child wins.

Of course it takes many years to find out whose child is the smartest and no one wants to wait. Because of their implicit belief in their ability to control outcomes, AP proponents don’t bother to wait. They simply compete on the basis that their children are going to be smarter than those of women who make different choices!

Attachment parenting is a parenting philosophy, but it is also a reflection of cultural assumptions and simple human competitiveness. AP proponents believe that they are fashioning superior children and have contempt for those who make different parenting choices. They assume, imply and often flat out assert that mothers who make different choices don’t care to give their children a competitive advantage. It hasn’t occurred to them that many mothers know that AP practices don’t give children a competitive advantage and indeed reject the notion that raising children has anything to do with competition.

I urge readers to submit a guest post. I’d love to give you a forum to be heard.

This article gives hope that we will be able to more accurately predict girls at risk to get them on training programs to reduce their excess risk of this serious athletic injury. 

From Medscape Medical News

Nomogram Predictive of Which Female

Athletes Are High-Risk for ACL Tears

Waterbirth dangers to newly born babies

by Amy Tuteur, MD

Waterbirth has become a central component of “natural” childbirth dogma, despite the fact that for primates giving birth underwater is entirely unnatural. You don’t need a medical degree to appreciate the idiocy of birth in water.  read more

The American Cancer Society has a nice discussion of DCIS.  It reads as follows:

Ductal carcinoma in situ

Ductal carcinoma in situ (DCIS; also known as intraductal carcinoma) is the most common type of non-invasive breast cancer. DCIS means that the cancer cells are inside the ducts but have not spread through the walls of the ducts into the surrounding breast tissue.

About 1 in 5 new breast cancer cases will be DCIS. Nearly all women diagnosed at this early stage of breast cancer can be cured. A mammogram is often the best way to find DCIS early.

When DCIS is diagnosed, the pathologist (a doctor specializing in diagnosing disease from tissue samples) will look for areas of dead or dying cancer cells, called tumor necrosis, within the tissue sample. If necrosis is present, the tumor is likely to be more aggressive. The term comedocarcinoma is often used to describe DCIS with necrosis.

It is not clear from what I can find whether Ms. Navratilova has comedocarcinoma or a less aggressive type of DCIS, but regardless she has a great prognosis.  Score one success for mammography. 

Of note Ms Navratilova fits some but not all of the typical risk factors for breast cancer. At 55 years old she is clearly in the age range at risk.  Breast cancer incidence increases with age.  She certainly is not obese and has had no lack of physical exercise, but women who have not had children are a slightly higher risk for breast cancer as are women who have not breast fed an infant, so Ms. Navratilova fits those aspects of a high risk profile.  Family history and estrogen use, either as oral contraceptives or postmenopausal hormone replacement therapy, are also risk factors.

1. Starting early with prevention of obesity is key. Once overweight it is far more difficult to prevent further weight loss. Multiple prior studies have demonstrated how difficult it is to achieve sustained weight loss.
2. Calorie restriction is needed to prevent weight gain once overweight. Exercise alone is not sufficient.

The conclusion of this study sums it up pretty well.

“In conclusion, in this large prospective study of women consuminga usual diet, sustained moderate-intensity physical activityfor approximately 60 minutes per day was needed to maintainnormal weight and prevent weight gain. These data suggest that the 2008 federal recommendation for 150 minutes per week, while clearly sufficient to lower the risks of chronic diseases, is insufficient for weight gain prevention absent caloric restriction.Physical activity was inversely related to weight gain onlyamong normal-weight women; among heavier women, there was norelation, emphasizing the importance of controlling caloricintake for weight maintenance in this group.”  JAMA. 2010;303(12):1173-1179

I like Hannaford’s comment, “I would never recommend that someone use the pill simply to reduce their risk of disease later in life,” he said. “However, if the choice is the pill, this decision does not increase a woman’s risk of long-term death. Indeed it may even have some benefits.”

Published 11 March 2010, doi:10.1136/bmj.c927
BMJ 2010;340:c927