✓ Member
Looking For Some Cholesterol Guidance
Not sure if this is the appropriate place for this, but I figure Jordan and Sully both hang out here from time to time.
Relevant Stats -
Male
32
170 lbs
5'-11"
Weak
Body fat is probably around 18%
My cholesterol is high - 275 total cholesterol. Both of my parents have high cholesterol, so I figure my genetics have pretty much shat on me. My HDL and ratios, however, are excellent -
275 total
174 LDL
79 HDL
110 Tri
I'm already on Dilantin for probably the rest of my life - I have a seizure disorder. The last thing I want is another pill to take every day - not to mention the myriad bad things about statins I hear around here and elsewhere.
I am sort of familiar with the research suggesting that high cholesterol is not necessarily bad, and that LDL comes in dense and fluffy, and that particle concentration is a better indicator of risk, etc. etc. Frankly, I wouldn't be at all concerned if my cholesterol were only a little high, but it's a lot high.
I'm just trying to figure out whether at 275, I should break down and try the doctor's advice (drugs), or push for more comprehensive (and expensive, I assume) lab tests. I'd like to continue my meager progress, but eating enough to recover and gaining a little fat along the way has me worried about increasing my cholesterol. I am aware that at 32 years old, my 10-year risk is <1%, but it still concerns me.
Any thoughts would be greatly appreciated.
Community Organizer (Administrator)
Treating lab values is a highly questionable practice (and that's before you get into problems with sampling).
To the extent you want to worry, look for *trends*, not at any particular result by itself.
Dilantin tends to increase levels overall, with increased HDL and decreases in LDL, so pay attention to changes in doses along with your lipids.
✓ Member
It's definitely a trend, one that took a hard left last year. My total cholesterol has always been a little high, typically around 215. Not high enough for my doctor to be concerned. Last year, after some time on SS and a poorly executed high-fat diet, I clocked in at 290. After some weight loss and cleaning up my diet, it's still high.
I've long suspected the Dilantin as a factor, although I figured it was due to its tendency to suppress insulin, increasing blood sugar and arterial inflammation (I'm talking out of my ass here). My fasting blood sugar in typically borderline, btw. My Dilantin levels have been pretty constant over the 12 years I've been on it.
I appreciate the response, Stef.
Member
Autopsy studies of teenagers show coronary artery plaques are already developing at that age. While in certain cases treating asymptomatic lab values isn't responsible, in the case of cholesterol it's asymptomatic until you have an MI, angina, a stroke, etc. If asymptomatic disease had no prognostic meaning then we wouldn't bother to check it.
Because you're young it's worth trying lifestyle changes, but they only work so well. We don't have much data on prevention of heart disease by treating someone for 20 years starting at age 32, but honestly do you want to go from 32 to 50 with an LDL of 175 or an LDL of 110? I made that choice myself - been on a statin since age 33 for almost the same numbers. And I hate taking medicines - but I'm an informed consumer and this was a no brainer for me.
Starting Strength Coach
Have you tried heavy/high aerobic / threshold anaerobic exercise? I'm not talking weightlifting (which you should be doing anyway), but hard aerobic activities like cycling (interval training) and / or pushing the prowler? Or running, if by running you mean 10 x 200m sprints with rest in between each.
Member
What's your diet like?
✓ Member
I've tried the lifestyle changes, and just like you've said, they only worked so well. Although, with all the seemingly conflicting information out there, I always have doubt in the specific changes that I made. In my case, I cut my fat intake in half (to around 90-110g daily. My macros are something like 100g fat, 300g carbs, and 225g protein, for reference), stopped eating eggs, increased my fiber to 30-40g a day, added in a little conditioning, and dropped 20+ pounds.Originally Posted by Paul1
I eat clean and unprocessed, with the exception of maybe a burger on a Saturday night. I think any further lifestyle changes would start impacting quality of life in a way I'm not sure I want.
My bike pretty much lives on a trainer, and I do intervals once a week. Family/work obligations limit me to 4 days a week - 3 days of weight training, and one for conditioning. I've considered dropping one day of weight training for an additional day of conditioning. Maybe that's worth a shot.
Member
Have you spoken to your doctors about changing over to Lamictal (Lamotrigine)? It has fewer side effects than Phenytoin (Dilantin).
Community Organizer (Administrator)
There are all sorts of problems with lipids and how that information is used in clinical practice. Treating the lab value doesn't address the cause/s of the thing being measured. It also doesn't address whether the thing being measured is directly relevant in disease or simply a marker associated with causes that affect both that value and disease.
The same types of issues also apply to drugs used to modify the values and drugs come with their own direct and indirect costs. There's plenty to look at regarding statin costs/benefits and plenty of discussion about those things - a interested guy like the OP sounds like the type to start looking at those things, find out what is out there & to weigh those risks, and make his own judgements.
http://www.health-heart.org/Point-Counterpoint.pdf
Member
Since you are an informed consumer and a medical expert as well, can you show the data suggesting LDL-c as a causative agent for Atherosclerosis and CVD?
From Ravnskov (2002):
‘The more LDL there is in the blood, the more rapidly atherosclerosis develops.’ This 1984 statement by the Nobel Award winners Michael Brown and Joseph Goldstein1 has dominated research on atherosclerosis since then. As shown here, this hypothesis appears to be falsified by the fact that degree of atherosclerosis, and atherosclerotic growth, were independent on the concentration or the change of LDL‐cholesterol in almost all studies. The role of LDL‐cholesterol for atherosclerosis growth has been exaggerated, a finding with consequences for the prevention of cardiovascular disease. For instance, as the statins exert their beneficial influence on the cardiovascular system by several mechanisms, it may be wiser to search for the lowest effective dose instead of the dose with maximal effect on LDL‐cholesterol. Neither should an elevated LDL‐cholesterol be the primary target in cardiovascular prevention, as recently claimed by the American National Cholesterol Education Program, and researchers should direct more attention to other hypotheses.
I may have overlooked studies that have found an association between changes of LDL‐cholesterol or other lipid fractions, and atherosclerotic progression. However, although the presence of exposure‐response is not sufficient proof in itself of causality, it is difficult to explain its absence.
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