FAQs

  • Protein minimums:

    1-1.5 grams per kg of body weight per day

    Or

    1 gram per pound of body weight

    Or

    5-7 grams (for weight maintenance) for every 100 calories you eat

    Or

    10 grams (to encourage fat loss) for every 100 calories you eat

    Protein powder - should contain at least 20g of protein per scoop/serving

    Avoid added sugars and artificial sweeteners

    NSF certified protein powders - google list

    Recommended brands: Drink Wholesome, Just ingredients, Jocko Molk, Momentous

  • Fiber minimums:

    Google "what does 30 grams fiber look like?"

    Aim for 30 grams a day or 15 grams for every 1000 calories you eat

    Raspberries (8g/cup), blackberries (8g/cup), avocado (10g), artichoke, beans (15g/cup), lentils/legumes (15g/cup)

    You may also use supplements like Metamucil, Benefiber, psyllium husk

  • FEMALES  Know your numbers: metabolic health indicators

    Waist circ: <35in 

    BP: <120/80

    Blood sugar: <100 fasting, or A1c <5.7%

    TG: <100

    HDL: >50 

     

    MALES  Know your numbers: metabolic health indicators

    Waist circ: <40in 

    BP: <120/80

    Blood sugar: <100 fasting, or A1c <5.7%

    TG: <100

    HDL: >40 

  • Basic concepts for resistance training:

    The goal is to build muscle mass.

    RPE (rate of perceived exertion) goal of 8-8.5.

    Each set should be 8-12 reps.

    At the end of each set you should have no more than 2 reps in reserve.

    REST is very important – 1-2 min rest between sets.

  • Daily: 30 - 30 - 30

    30 min exercise per day

    30 grams of fiber per day

    30 grams of protein per meal

  • Coronary atherosclerosis is a ubiquitous process that occurs in the vast majority of humans if they live long enough, regardless of lifestyle. This is a product of exposure over time, or area under the curve if you will, to plaque forming lipoproteins along with other vascular insults that occur naturally during our lives. Yes, poor lifestyle can accelerate or worsen the process. Yes, healthy lifestyle can help. However, that’s just not the whole picture.

  • There are several different types of heart attack. However, the most life-threatening type is one that occurs due to plaque rupture meaning the non-calcified lipid core of the plaque breaks out from under the inner layer of the artery wall and blocks off the lumen of the vessel acutely.

  • There are several different types of stroke. However, a common cause of stroke is plaque rupture, the same mechanism as with heart attack. In this case, the non-calcified lipid core of the plaque breaks out from under the inner layer of the artery wall and blocks off the lumen of the vessel acutely.

  • Atherogenic lipoproteins, more colloquially know as cholesterol, are a major risk factor for plaque formation and cardiovascular disease. They should be treated based on your risk level and not only when disease becomes visible. If we wait until disease is visible, we are behind. An example: blood pressure is a significant risk factor for plaque formation as well, but you don’t wait to treat your blood pressure until you have a stroke or your CAC score is >zero.

  • Very few people have a low enough atherogenic lipoprotein burden (think apo B containing particles like LDL) that they need less than a 15-20% reduction to achieve a level at which plaque formation would be halted. Lifestyle changes generally only afford a 15-20% reduction, hence the need for additional lower by a different mechanism (enhanced LDL clearance) with medication. The most effective approach a halting plaque production is with both lifestyle and medication.

  • Apolipoprotein B (apo B), more specifically apo B-100, is the main structural protein on atherogenic (plaque forming) lipoprotein particles such as low-density lipoprotein (LDL), very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and lipoprotein (a). It is a more accurate marker of atherogenic risk than LDL alone because its measurement encompasses risk conveyed by other atherogenic molecules aside from LDL.

  • Lipoprotein (a) or Lp(a) is a plasma lipoprotein that is comprised of a cholesterol-rich LDL particle that contains one molecule of apolipoprotein B-100 (apo B-100) attached via a disulfide bond to an additional protein, apolipoprotein (a) (apo(a)). Lipoprotein (a) is an inherited risk factor for cardiovascular disease including, but not limited to coronary artery disease, peripheral artery disease, aortic stenosis, heart attack, stroke, and death from cardiovascular disease. It does not change significantly with diet, lifestyle, or medications. It is set by about the age of 5 and therefore leads to exposure to this atherogenic molecule for most of life. Optimizing modifiable risk factors such as LDL and apo B is crucial to offset risk of Lp(a). 75 nmol/L is the cutoff for normal and above 125nmol/L is when it is considered a significant risk factor. Everyone should be screened for elevated Lp(a).

    Familyheart.org/high-lipoprotein-a

  • Each 39mg/dL reduction in LDL translates to 22% risk reduction of cardiovascular events (heart attack, stroke, death from those things) over 5 years and >50% if maintained for decades.

  • Weight Loss

    Event small amounts of weight loss can reduce triglycerides and likely increase HDL.

    Lose 3-8% of your total body weight can reduce LDL by 5%, but this is not always a reliable tool.

     

    Exercise

    This will reliably reduce triglycerides as well as increase HDL.

    Exercise does not reliably decrease LDL.

     

    Diet – This is your big lifestyle level to pull for LDL. Each intervention can lower LDL by about 5% and the effects can be additive to an extent. Generally, significant dietary change can lead to a 15-20% reduction in LDL.

    Increase fiber: whole oats, barley, avocado, berries, legumes, beans, psyllium

    Increase mono- and polyunsaturated fats: avocado, nuts, seeds

    Decrease saturated fat: butter, lard, animal products (meat, cheese, eggs), fried foods

    Increase plant protein intake: legumes, beans, nuts, seeds, tofu, tempeh, whole grains

    Incorporate plant sterols and stanols: nuts, seeds, whole grains (particularly rye and wheat), legumes, avocados, apples, broccoli, Brussels sprouts

     

    Supplements – Generally we don’t see more than a 5% decrease in LDL with supplements.

    Red yeast rice: statistically significant LDL lowering, but not more than 5% reduction which is not clinically significant. This supplement contains lovastatin (a naturally occurring statin). It can be harmful to the kidneys because concentrations/dose is not monitored/consistent.

    Plant sterols: statistically significant LDL lowering in studies, but not more than 5% reduction which is not clinically significant. These can dangerously increase some people’s LDL. Be careful with these.

    Berberine: seems to modestly lower LDL in some people, can have GI side effects, should be avoided in liver disease

    Pine bark: reportedly lowers LDL, raises HDL, but studies inconclusive and side effects can occur

    Omega 3s: these are NOT an LDL lowering supplement. They can lower triglycerides modestly in some people depending on the person and the supplement formulation.

    Niacin: this is NOT recommended. Side effects are common, often severe, and can be dangerous. Guidelines recommend against the use of this supplement and prescription for LDL lowering / HDL increase.

    *Be careful here. Supplements are not FDA monitored and can be harmful/toxic. They can and often interfere with the metabolism of other medications/supplements. They can also generate side effects, some of which are very serious. Just because they are over the counter does not mean they don’t require monitoring or thought surrounding their use. Always discuss any supplements with your healthcare provider to be sure there are no known risks in your case.

     

    Medications

    Bile acid sequestrants: routinely lower LDL by 15-30%, but have frequent and unpleasant side effects. Not used much anymore.

    Statins: routinely lower LDL by 30% (this is often true even at very small doses a few days a week) and up to 50% (often with just the starting dose daily, but reliably at moderate doses). They also lower triglycerides 7-30%.

    Ezetimibe: routinely lowers LDL 15-20%

    Bempedoic acid: routinely lowers LDL about 30-35%

    PCSK9 inhibitors: routinely lowers LDL 50% or greater

    All medications for LDL lowering increase LDL clearance (removal of LDL from circulation) but by a variety of different mechanisms. Combining mechanisms can be extremely effective. All lipid lowering drugs on the market are safe. Many have been used for several decades.

    Fenofibrate: lowers triglycerides up to 50%. Indicated to prevent pancreatitis when fasting triglycerides are >500mg/dL.

    Omega-3-acid ethyl esters: prescription triglyceride lowering medication, indicated to prevent pancreatitis when fasting triglycerides are >500mg/dL.

    Icosapent ethyl: this is a mild triglyceride lowering medication but seems to have clinically significant ASCVD risk reduction in patient populations who meet use criteria.

  • No. Statins and other lipid lowering therapies help treat risk for atherosclerosis, the cause of approximately 30% of dementia (vascular dementia). Many people are put on statins when they have a heart attack or stroke and not long after, also see signs of dementia. They assume the statin was the cause. It was not. Dementia begins decades before it becomes clinically apparent. Dementia is often the same disease process (vascular dementia is due to atherosclerosis) presenting in a different organ system. Treating risk earlier in life helps prevent dementia, not cause it.

  • Statins have been associated with small increases in A1c (average blood sugar estimate over 90–120-day time frame) on the order of 0.1-0.3%. For example, A1c increasing from 6.2% to 6.5% after statin initiation. This person had prediabetes to begin with and crossed over the arbitrary line into diabetes with the A1c of 6.5%. The problem of insulin resistance is not worsened at a clinically relevant magnitude but catches attention because the patient is then labeled differently. This change in A1c is usually not even brought up in conversation when it is still within the realm of normal, for example, 5.1-5.4%. The risk of forgoing treatment of a major risk factor such as hyperlipidemia, especially in an already prediabetic patient, far outweighs the risk of slightly increasing blood sugar.