Atherosclerosis is responsible for half the deaths in the US today! If you get it in your coronary arteries, you’re at risk for myocardial infarction; if it’s in your carotid arteries, you’re at risk for stroke. And lest you think this is something you don’t need to worry about until you’re old, you should know that this process starts very, very early in life – somewhere during childhood – and you just can’t tell you have it until you suddenly start getting nasty symptoms (doctors call this the “clinical horizon,” which sounds strangely picturesque). Scary.
There are lots of risk factors for getting atherosclerosis. They are divided into two groups: major risk factors (which are known for sure to cause atherosclerosis) and lesser or uncertain risk factors (which have less of an effect, or are as yet unproven). Let’s take a look at both groups.
Major risk factors
Some of the major risk factors for atherosclerosis you are simply stuck with, and there is not a thing you can do about them. These include:
- increasing age (atherosclerosis is more common as people get older)
- gender (At younger ages, males are more at risk. Premenopausal women are relatively protected; after menopause the risk in women increases and eventually exceeds the risk in males.)
- family history
- genetic abnormalities (lots of these probably exist; many aren’t fully understood).
The good news is that there are several major risk factors that you can potentially do something about. These include:
- Hyperlipidemia (best thing to do is have a high level of HDL cholesterol, which actually scavenges lipids and removes them from atherosclerotic plaques, and a low level of LDL, which is the “bad” cholesterol that makes up part of the plaques.
- Hypertension (there’s no one right number, but it should be at least below 140 systolic and 90 diastolic)
- Cigarette smoking (smoking potentiates the other risk factors)
- Diabetes (patients with diabetes mellitus have an increased amount of atherosclerosis at a younger age)
- C-reactive protein level (this is a serum marker of inflammation; the higher the level, the greater the risk for atherosclerosis)
Lesser or uncertain risk factors
Then there are a bunch of other things that may be related to an increased risk, but the data is not yet conclusive. These include:
- Obesity
- Physical inactivity
- Stress
- Postmenopausal estrogen deficiency
- High carbohydrate intake
- Lipoprotein (a) (an altered form of LDL that seems to be independently associated with increased risk of atherosclerosis)
- Trans-fat intake
- Chlamydia pneumoniae infection (Chlamydia pneumoniae and other bugs have been detected in plaques but not in normal arteries, and there are increased antibody titers to C. pneumoniae in patients with more severe atherosclerosis. But a causal link hasn’t been established.)
So: don’t smoke; eat well (not too many carbs, no trans fats), exercise, and maintain a healthy weight; keep your blood pressure and lipids within the normal range; if you have diabetes, work to keep it as controlled as possible; don’t get Chlamydia pneumoniae. Oh, and don’t get all worried about it – stress is another potential risk factor!
Image credit: Hamed Masoumi (http://www.flickr.com/photos/hamedmasoumi/2266654041/), under cc license.
One of the things that researchers are studying like crazy is the process by which cancer takes root and grows in the body. Our diet plays a huge role in this process (witness the much lower incidence of cancers in India, for example, despite the much higher incidence of carcinogens!). Â For your own health, and for the health of your future patients, I highly recommend David Servan-Schreiber’s book, Anticancer: A New Way of Life, which came out last year. David is an MD who developed brain cancer and went through successful medical treatment. However, his tumor recurred, and at that point he decided he needed to change his way of life. This book describes the effects diet and stress have on the growth of cancer – and before you blow that off as being too foofy or alternative, you should know that he backs up every point he makes with tons of research from accomplished scientists at respected places like Harvard and M.D. Anderson. Much of this post is from information described in David’s book.
The process of tumor growth is much like the growth of weeds. Tumors grow in three phases: 1) initiation, 2) promotion, and 3) progression. Initiation is the phase when a seed settles in the soil, promotion is the phase when the seed becomes a plant, and progression is the phase when the plant becomes a weed (developing beyond control, invading flower beds and growing right up to the sidewalk).
Initiation (the planting of the seed) depends largely on our genes and on toxins (radiation, carcinogens, etc.). But promotion (the growth of the seed) depends on having the right survival conditions: favorable soil, water, and sun. The cool thing is that promotion is reversible! If you can change the tumor’s environment, you can prevent it from spreading. Diet plays a role – probably a big role – in the creation of a favorable vs. unfavorable tumor environment.
Cancer “fertilizers”
Here are some dietary substances that create a fertile soil for cancers:
Refined sugars (drive up proinflammatory insulin and insulin-like growth factor, or IGF)
Insufficient omega-3s/excess omega-6s (favor inflammation)
Growth hormones in meat and non-organic dairy products (stimulate IGF)
Okay, what diet does this sound like? Lots of sugar, bad fats, and meat – the typical Western diet.
Cancer inhibitors
So, what should we eat? In addition to avoiding saturated fat, sugar, meat and non-organic stuff, a good cancer-fighting diet would include some/all of the following:
Catechins (in green tea) – inhibit angiogenesis
Phytoestrogens (in soy products) – block overstimulation of tumors by estrogen; prevent angiogenesis
Curcumin (in turmeric) – inhibits inflammation, inhibits angiogenesis, promotes apoptosis in tumor cells
Ellagic acid (in berries) – inhibits angiogenesis, blocks transformation of environmental carcinogens into toxic substances
Anthocyanidins (in blueberries, cranberries, cinnamon, dark chocolate) – promote apoptosis in tumor cells
Terpenes (in mint, thyme, marjoram, oregano, basil, rosemary) – inhibit tumor cell invasion, promote apoptosis in tumor cells, inhibit angiogenesis
Gingerol (in ginger) – inhibits inflammation and angiogenesis
Sulforaphane, indole-3-carbinol (in cruciform veggies) – prevent precancerous cells from becoming malignant; promote apoptosis of tumor cells, inhibit angiogenesis
Sulfur compounds (in garlic and onions) – reduce carcinogenic effects of nitrosamines (created in overgrilled meat and present in tobacco); promote apoptosis in tumor cells; help regulate blood sugar levels.
Lycopene (in carrots, yams, other bright colored veggies and fruits) – stimulates NK cells to become more aggressive; inhibits tumor cell growth
Long-chain omega-3 fatty acids (in fatty fish) – reduce cancer cell growth, prevent metastasis
Vitamin D (sun, cod liver oil, milk (tiny amount), vitamins) – dramatically reduces risk of several cancers
Polyphenols (red wine, chocolate) – block NF-kappa B (important in all three stages of cancer development: initiation, promotion, progression), limit angiogenesis
Photo credit: L’eau Bleue (http://www.flickr.com/photos/8175535@N05/3536354514/), under cc license.
When people talk about immunodeficiency states, they’re usually talking about secondary immunodeficiencies, like AIDS.
The primary immune deficiencies really don’t get much press. Which is unfortunate, because although they are much less common than secondary immune deficiencies, they still occur, and it’s important to understand them for that reason alone. Plus, they are very testable – either on board exams, or on class exams.
Time is short, though, and you need to know the basic points for each one without having to wade through a lot of chapters in a textbook. So, without further ado, here is a short, bullet-pointed list of the main disorders, with particular emphasis on the part of the immune system that is affected, and the clinical manifestations of the disease.
X-linked agammaglobulinemia
- Pre-B cells can’t differentiate into B cells
- Patients have no immunoglobulin (Ig)
- X-linked (so seen only in males)
- Presents at 6 months of age (when maternal Ig runs out)
- Patients get recurrent bacterial infections
- Treatment: intravenous pooled human Ig
Common variable immunodeficiency
- Group of disorders characterized by defective antibody production
- Affects males and females equally
- Presents in teens or twenties
- Basis of Ig deficiency is variable (hence the name) and often unknown
- Patients more susceptible to infections, but also to autoimmune disorders and lymphoma!
Isolated IgA deficiency
- Most common of all primary immune deficiencies
- Cause is unknown
- Most patients asymptomatic
- Some patients get recurrent sinus/lung infections or diarrhea (IgA is the major Ig in mucosal secretions)
- Possible anaphylaxis following blood transfusion (patients have anti-IgA antibodies, and there is IgA in transfused blood!)
- Increased incidence of autoimmune disease (who knows why)
Hyper-IgM syndrome
- Patients make normal (or even increased) amounts of IgM
- But can’t make IgG, IgA, or IgE!
- X-linked in most cases
- Patients also have a defect in cell-mediated immunity
- Patients have recurrent bacterial infections and infections with intracellular pathogens (e.g., Pneumocystis jiroveci)
DiGeorge syndrome
- Developmental malformation affecting 3rd and 4th pharyngeal pouches
- Thymus doesn’t develop well
- Patients don’t have enough T cells
- Infections: viral, fungal, intracellular pathogens
- Patients may also have parathyroid hypoplasia
- Treatment: thymus transplant!
Severe combined immunodeficiency
- Group of syndromes with both humoral and cell-mediated immune defects
- Patients get all kinds of infections
- Lots of very different genetic defects
- Half of cases are X-linked
- Treatment: bone marrow transplantation
The best way to remember these might be to make a little chart, with the diseases in one column, and subsequent columns for transmission (X-linked or not), immunologic defect (e.g., no immunoglobulin production), and clinical features (e.g., infant with recurrent bacterial infections).
If you read this post about hemolytic disease of the newborn, you already know the answer: it’s used for determining the amount of fetal blood that has backed up into the mom’s circulation.
It’s usually done for the purpose of determining Rhogam dose. You need to make sure you give enough Rhogam to suppress the mom’s immune response. If there has been a little bleed, you give a little; if there has been a big bleed, you need to give more. Take a look at this chart if you want to know exact doses.
Here’s how it’s done:
1. Prepare blood smear from mom’s blood.
2. Expose blood smear to acid bath (this removes adult hemoglobin, which is acid-sensitive) but not fetal hemoglobin.
3. Stain smear. Fetal cells appear dark pink; maternal cells look like “ghosts.” Here’s what this looks like:
4. Count lots of cells and report percentage of cells that are fetal (specifically: you count the number of fetal blood cells per 50 low power fields. If you see 5 cells per 50 low power fields, that’s equivalent to a 0.5 mL fetomaternal hemorrhage).
If you want to get really fancy, you can look for fetal blood cells using flow cytometry. Using a sample of mom’s blood, apply an anti-HbF (fetal hemoglobin) antibody, and then run the sample through the flow cytometer. In the little printout, look for cells that stain intensely with HbF: these are baby’s cells! A few of mom’s cells will have weak HbF staining – this is normal in adults.
Top image credit: adamr.stone (http://www.flickr.com/photos/adamrstone/3098924060/) via cc license.
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