Maternal Hyperlipidemia, Hypercholesterolemia, Hypertriglyceridemia

Hyperlipidemia or hyperlipemia is an excess of fat or lipids (triglycerides and/or cholesterol) in the blood. 

It can be primary, due to a genetic error in fat metabolism (familial combined hyperlipidemia, familial dysbetalipoproteinemia, familial hypercholesterolemia, familial hypertriglyceridemia), or secondary to poor diet (excessive consumption of saturated fats), lack of regular exercise, some medications, alcoholism, diabetes, hypothyroidism, lupus erythematosus, kidney disease or polycystic ovarian syndrome. ^{(MedlinePlus 2023)}

Hyperlipidemia causes accumulation of fat, cholesterol and other substances in the walls of the arteries, or atherosclerosis, which increases the risk of angina and myocardial infarction, stroke and other circulatory problems. ^{(MedlinePlus 2022)}

Before and in addition to taking lipid-lowering drugs (which lower fat levels in the body), the first step in treatment is to eat a diet low in saturated fat and refined sugar and to exercise daily. ^{(MedlinePlus 2020)} 

The problem of treating hyperlipidemia during lactation is that infants need cholesterol for the development of brain tissue, myelination of nerves and it is also the basis of many enzymes.

Some authors and expert consensus advise postponing statin treatment from 3 months before pregnancy and until breastfeeding ends or is not exclusive ^{(FDA 2021, Shala 2020, Lawrence 2016 p 393)}, since except in severe forms of hypercholesterolemia ^{(Moss 2018)}, postponing drug treatment for a few months is not likely to alter the long-term outcome of the disease in the mother ^{(FDA 2021)}.This is due to the fear that the drugs taken by the mother could reach the infant through breast milk and lower its cholesterol levels and/or that these drugs could lower the concentration of breast milk cholesterol.

But other expert authors consider safe or probably compatible or of minimal risk the use of lipid-lowering medication such as statins, especially the hydrophilic ones rosuvastatin or pravastatin, during pregnancy and/or breastfeeding (Hale, Botha 2018, Holmsen 2017, Amir 2011) because: 

1. Most lipid-lowering drugs are thought very likely or known with certainty not to be excreted in breast milk or to be excreted in negligible amount because of high molecular weight and/or high plasma protein binding and/or high volume of distribution and/or not absorbed in the intestine.
2. Mothers homozygous for familial hypercholesterolemia (FH) took statins during 18 pregnancies and 11 breastfeedings of 3 to 9 months duration and their infants had no developmental or school learning problems ^{(Botha 2018)} and there are no published data indicating that statins taken by the mother during breastfeeding are harmful to the nursing infant ^{(Holmsen 2017)} nor that statin use during pregnancy increases the risk of birth defects or miscarriage. ^{(FDA 2021)}
3. Although 102 women affected by FH stopped taking statins for a mean of 2.3 years (range 0 to 14 years) for the times of pregnancy and breastfeeding without it being known whether this increased the risk of cardiovascular disease ^{(Klevmoen 2021)}, it is known that hypercholesterolemia maintained during pregnancy in a woman with FH increases the risk of atherosclerosis in the child ^{(Napoli 1999)}, that these women develop very high cholesterol levels during this period ^{(Holmsen 2017, Avis 2009)} and that there is an increase in arterial intima media thickness during pregnancy in women with FH who do not take medication. ^{(Kusters 2010)} 
4. Normal breast milk cholesterol concentration ranges from 30 mg/dL in colostrum to 10 - 20 mg/dL in mature milk ^{(Lawrence 2016 p98, 105 and 767)}. Cholesterol levels are normally increased (by 40%) during pregnancy and lactation in healthy women ^{(Lawrence 2016 p590)}. Milk cholesterol numbers are very stable even in hypercholesterolemic women and are not severely affected by diet or the mother's nutritional status, leading to the assumption that milk cholesterol is synthesized, at least in part, in the mammary gland ^{(Lawrence 2016, p 289-90)}. For all these reasons, it is very unlikely that hypolipidemic medication is able to alter the lipid composition of milk.
5. Cholesterol concentration is greatly increased (up to 3-fold) in the milk of lactating mothers affected with familial hypercholesterolemia in homozygous form ^{(Holmsen 2017, Tsang 1978)}. Statin treatment would at most reduce it to normal levels. ^{(Holmsen 2017)}
6. Breastfeeding has a cardioprotective effect: it reduces the risk of myocardial infarction and hypertension, improves blood glucose control and lipid profile, and reduces the risk of type 2 diabetes , which is particularly important for women with FH and their infants. ^{(Holmsen 2017)}
7. The health benefits of a woman with FH continuing to breastfeed while using a statin outweigh the low risk to the child. It is safe and beneficial for infants of women with FH to be breastfed while the mother is receiving adequate treatment with a statin, preferably rosuvastatin. ^{(Holmsen 2017)}
8. Breastfed infants have higher plasma cholesterol levels than those fed artificial formula and this would protect them against the consequences of hypercholesterolemia in adult life ^{(Lawrence 2016 p108)}. Infants fed formula substitutes ("artificial milks") do not receive cholesterol in their diet, as these products do not contain cholesterol ^{(Lawrence 2016 p 109 and 215)}. The amount of cholesterol in breast milk that would remain after the hypothetical cholesterol reduction produced by the statins taken by the mother would still be much higher than that contributed by artificial formulas. ^{(Holmsen 2017)}

In conclusion, it seems wise to advise mothers with severe FH to continue statins and/or other lipid-lowering drugs during lactation. Mothers without FH and with moderately high cholesterol levels can discontinue treatment during the lactation period by monitoring their low-density lipoprotein (LDL) levels.

See below the information of these related groups:

• ATC C10AA: Lipid Modifying Agents HMG CoA reductase inhibitors (Statins)
• ATC C10AB: LIpid Modifying Agents. Fibrates
• ATC C10AC: Lipid Modifying Agents. Bile acid sequestrants
• ATC C10AD & C10AX: Nicotinic acid and derivatives, and Other lipid modifying agents