pregnancy blood pressure Archives

Pregnancy Toes – What Sugar Does to Feet

Published on December 28, 2020

13559 views

Pregnancy toes are really swollen feet and swollen toes. The name stuck in my mind because one of my daughter-in-laws is pregnant and I was sent a photo from her winter vacation in her flip flops in the snow and winter coat—she was not able to put her boots on because of her swollen feet (swollen even in the cold!).

I did not think much about it until she came to visit me yesterday and I noticed the flip flops and her chubby toes. She had “pregnancy toes” again she said. It then suddenly all became clear. I asked her: did you by any chance have any sugar today? And she said “as a matter of fact, yes!”

I reached for my salt pills that I use for my migraines as do all members in my migraine group on Facebook and handed her one. I really should have photographed what happened but I did not think the effect was going to be so fast and so big. Less than 15 minutes after she took the salt pill and a glass of water, her toes went back to normal. We ended up laughing it away. Had she known this, she could have worn her boots in the snow after all!

So what did her pregnancy toes have to do with sugar and salt you may ask? Previously, I quoted from the Harrison’s Manual of Medicine an important paragraph that I repeat here:

…serum Na+ falls by 1.4 mM for every 100-mg/dL increase in glucose, due to glucose-induced H2O efflux from cells. (page 4)

The above means glucose (part of sugar) and sodium (part of salt) are in inverse relationship. As you increase sugar, salt drops and water is sucked out of your cells by sugar like a giant Slurpee machine. The water then collects on the outside of your cells rather than the inside, thereby dehydrating your cells and at the same time make your body swell. Edema is often associated with too much salt, but in fact, it is too much sugar. Being always thirsty is associated with Type 2 Diabetes but it is also associated with not having enough salt in the body since without salt the cells cannot get hydrated.

In light of this fragile balance between sodium and glucose in the blood, are we treating pregnancy edema, gestational diabetes, and other maternity complications, the way we should? Consider that with pre-eclampsia (gestational hypertension), women are told not to eat salt. You can see what happens when we reduce sodium: glucose increases and we also induce an ionic imbalance. This ionic level imbalance is visible (like the swollen toes) and may lead to further complications. There are two problems that we are facing here: first if she does not eat salt, her sodium-potassium pumps cannot work–this may cause migraines and headaches as I often see in my migraine group. Secondly, as you saw the fragile balance between the see-saw action of glucose and sodium, if she stops eating sodium her glucose may increase, causing swelling. This is an interesting theory to ponder – one that merits research.

Sodium and Glucose Work Together

Salt breaks up in the body into sodium and chloride. Sodium attracts water and holds onto it inside the cells. It keeps chloride outside of the cells to ensure proper voltage and electrolyte balance with the aid of potassium. When you eat sugar, the glucose part of it removes the water from the cells via osmotic channels that are too narrow for the sodium ions to exit. Thus, one ends up with a ton of water outside the cells with sodium inside hugging a tiny amount of water. Swelling occurs as the water leaves the cells but remains between cells.

Given the inverse nature of glucose and sodium in the blood, if one is swollen as a result of too much sugar, eating salt will take the water back from sugar and move it back into the cells–as it did for my daughter-in-law’s pregnancy toes. What is important in this information is this:

If you feel swollen after eating sweets, you need to eat salt and drink a bit of water to reduce your swelling.
If you have Type 2 Diabetes or are hypoglycemic, eating a salty meal can give you a major sugar crash and land you in the hospital!
Eating sugar of any quantity will dehydrate your cells and you and make you run to the toilet every 30 minutes.

Because glucose takes water out of the cells, the edema that follows increases extra-cellular water and causes swelling in the body. This extra-cellular water needs to be reabsorbed into the circulation for the kidneys to be eliminated. To be reabsorbed, sodium is necessary since without sodium, the cells cannot operate their voltage gated sodium pumps and so the gates cannot open to grab glucose to take it into the cells and to get the water back into the cells. I think you can already see the contradictions in the logic of reduced salt: the mom-to-be is told to not eat salt, this causes extra-cellular water and swelling, which needs salt to be reabsorbed into her cells for clearance by the kidneys but which she is not allowed to eat. This way ionic level balance is not possible and chain reactions may occur with negative consequences. She may have protein leaching into her urine, extra hard kidney work, and a whole other long chain of complex events may kick in to make pregnancy a rather unpleasant experience risking the health of the fetus.

The amount of extra-cellular water is very hard for the body to get back into circulation without salt and may take days, taxing the kidneys with the volume of water leaving and increasing pressure on the blood vessels from the outside, causing high BP. However, as the volume of water is leaving the body finally, this reduces blood pressure. When a pregnant woman’s blood pressure drops as a result of all that water leaving, the dehydrated blood cells carry less oxygen. This indicates reduced oxygen for both her and the baby.

By telling mothers to reduce salt intake, glucose increases, which increases blood pressure (BP) rather than reduces it. The similar phenomenon happens in gestational diabetes. In gestational diabetes (and gestational hypoglycemia as well) the sugar level is unstable and is either too high or too low, respectively. Should the mother-to-be eat a salty pickle (as cravings always dictate pickles), she may end up in a major sugar crash and in the hospital for immediate treatment.

The balance between sodium and glucose is very fragile and extremely quick changing as you could see on my daughter-in-law’s foot. Interestingly we now also know that salt does not increase blood pressure but sugar does and so a reduced salt diet automatically increases blood pressure because of the glucose and sodium inverse connection and sugar’s dehydrating properties. Reduced salt also increases triglycerides (Graudal, 2011), causing a lot of problems for people with preexisting heart conditions. So by reducing the salt intake of the mothers to be, are we creating diabetic mothers and/or babies? Babies have been born with diabetes 2!

Is it possible that we are giving the wrong advise to pregnant women about salt and sugar? It’s an interesting question to pose and further research is badly needed. Knowing that salt and sugar are in inverse proportion in the blood, one may suggest eating them together. In fact, eating them together is a much better idea than eating sugar alone. It is best to not eat sugar at all but if you must eat sugar, consider eating salt too.

Sources:

Effects of low sodium diet versus high sodium diet on blood pressure, renin, aldosterone, catecholamines, cholesterol, and triglyceride. Graudal et al., Cochrane Database Syst Rev. 2011 Nov 9; (11).

This article was published originally on Hormones Matter on February 15, 2015.

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Pregnancy Hypertension

by Chandler Marrs, PhD

Published on February 24, 2015

3292 views

Every now and again I have the great pleasure of stumbling upon a brilliant piece of research; research that shakes the very core of medical science. Sadly, this is not one of those times. No, with the research I write about here, I cannot help but wonder why? Why was this study conducted? Why was it funded? Why was it published in such a prominent journal? And perhaps most importantly, why are there 15, well-credentialed, and likely, very highly accomplished individuals, lending their names to such a weak piece of research? Did they not read the study?

Just last month, published in the esteemed The New England Journal of Medicine, whose impact factor (54) far exceeds most journals in the space by a factor of 10, published a purportedly seminal piece on pregnancy hypertension: Less-Tight versus Tight Control of Hypertension in Pregnancy. The study was a huge, presumably well-funded (through a grant from the Canadian government), multi-center, international, randomized controlled trial set to investigate the important topic how best to treat pregnancy hypertension.

Pregnancy Hypertension

Hypertension during pregnancy is a growing problem that brings with it substantial risk to maternal and fetal health. How to treat pregnancy hypertension is of critical importance but not a single anti-hypertensive medication on the market currently has been tested for safety on pregnant women. Few data exist to evaluate the risks of taking such medications on short-term maternal or fetal health and no data exist to identify long term consequences. Not even the most basic of studies, those that evaluate drug pharmacokinetics and delineate appropriate dosing have been conducted for pregnancy (or any other complex hormonal environment).

Drug disposition and metabolism are altered significantly by pregnancy when hormone concentrations, plasma volume, enzymes, binding proteins, liver and kidney function change radically. These changes impact drug dosing and safety. Without proper consideration for these variables during pregnancy, the potential for overdosing and mis-dosing is significant, increasing the possibility of evoking serious maternal and/or fetal ill-effects. Setting aside the question of whether medications should be given at all during pregnancy (I don’t think they should be), I think we can all agree that when medications are necessary, safety and efficacy data must exist prior to administration.

It is from this perspective, that I approached the current study; a long overdue investigation about the safety and efficacy of anti-hypertensive drugs during pregnancy. Boy was I disappointed. In fact, the authors state: “We did not collect information on common adverse effects of anti-hypertensive medications…” In fairness, however, other important outcome data were collected, but the design of the study was so arbitrary that any potential insight these outcomes might have contributed, was lost.

Study Details

The current study asked whether controlling maternal blood pressure strictly within a pre-defined range of parameters provided better or worse maternal or fetal outcomes compared to a more flexible approach with a broader range of accepted blood pressure metrics. For the tight control group, the goal was to maintain diastolic blood pressure at or below 85 mm Hg. For the less tight group, diastolic pressure was to be maintained at or below 100 mm Hg. The study accepted medicated and non-medicated hypertensive women (n = 987, 56-58% were medicated from each group prior to entering the study), who were anywhere from 14 weeks of pregnancy through 33 weeks pregnancy (mean = ~23 weeks).

Once participants were enrolled into the study, decisions regarding whether to medicate (if not previously medicated), which medication to use, and at what dosages, were left to the providing obstetrician’s discretion. The study excluded women who, at the time of admission into the study, showed signs of pre-eclampsia, demonstrated high systolic blood pressure (>160 mm Hg), had pre-gestational diabetes, renal disease or were utilizing ACE inhibitors (angiotensin-enzyme-converting enzyme inhibitors). If these conditions developed subsequently, patients remained in the study.

The primary outcome variables included: pregnancy loss (miscarriage, ectopic pregnancy, elective termination, perinatal death), high level of neonatal care for greater than 48 hours, gestational age and weight at delivery and a range of neonatal complications. Secondary outcome variables, measured at a much more rigorous statistical significance level (p>.001) compared to the primary variables (p>.05) included: serious maternal complications (uncontrolled hypertension, transient ischemic attack or stroke, pulmonary edema, renal failure and transfusion), placental abruption, severe hypertension (>160 mm Hg systolic or >110 mm Hg diastolic blood pressure), pre-eclampsia or abnormal labs indicative of incipient pre-eclampsia.

Results

The reported results of this study were as follows:

There were no between group differences in either maternal or fetal complications.
Women in the less tightly controlled group had higher blood pressure.

So for all of the money and time spent, we learned that anti-hypertensives do, in fact, reduce blood pressure, and that how intensely one uses these medications has no statistical bearing on this particular set of outcomes. This is not to say that there were not negative outcomes. There were plenty in both groups of participants; from severe maternal hypertension, pulmonary embolism and pre-eclampsia, to serious neonatal complications and fetal death. There were simply no statistically identifiable differences in the rates of these complicatiosn between the two groups. In other words, both groups had similar rates of negative outcomes.

Flaws in Study Design

Why weren’t there any statistically relevant differences between the two groups? The answer to this question involves study design and herein we have a number of problems. First, the participant pool was largely hypertensive and medicated before entry into the study, providing no real control group from which the assess differences between blood pressure and outcomes in unmedicated versus medicated women. Elevated blood pressure is a significant risk factor for a number of maternal complications but so too are medications. What is the risk/benefit calculus that determines when the inherent risks of medications during pregnancy are outweighed by the risks of maternal blood pressure? In other words, when should we medicate to control hypertension? Delineating between the dangers of the blood pressure versus those of the medication would have been more telling. Admittedly, such a study would present ethical considerations and quite possibly could have only been done retrospectively. Nevertheless, without these types of data, it is impossible to discern either the safety or efficacy of any therapeutic intervention; effectively nullifying the results from the onset.

A second methodological problem is the failure to address statistically pre-existing health conditions and environmental variables that confound results. That is, we don’t know what portion of the overall negative outcomes might be attributable to pre-existing or even extraneous maternal health issues versus medication use or blood pressure control. For example, a good percentage of the women in both groups were not only medicated prior to entry into the study but were significantly overweight pre-pregnancy, smoked and/or had additional health considerations. These variables would independently impact maternal and fetal outcomes, but also, could additively or synergistically influence blood pressure and other maternal risk factors. Although the mean data for both groups were presented, no analyses that might provide a richer understanding of the relationship between blood pressure and perinatal outcomes was given.

Perhaps the most problematic aspect of this study was the failure to analyze data regarding the types and dosages of medications relative to the negative outcomes. Though the researchers collected medication data and reported some of those data in the supplementary appendices (number of women per group who took a particular type of medication absent dosages was reported), there were no analyses presented. This made it impossible to identify whether certain medications were more dangerous than others and would account for the observed negative outcomes in either group. Neither did this report tell us about the dose-response relationship relative to effective blood pressure management versus adverse reactions – a very basic calculation – nor did they tell us about the role of medication interactions in the observed negative outcomes.

What Value is This?

From the standpoint of a practicing physician, a researcher or a patient, what use is a study on medication safety and efficacy during pregnancy, if there are no analytics delineating dose-response relationships by medication(s) and risk factor? Is one medication safer than the others? Does a particular medication work better or worse for a specific group of women? Are there anti-hypertensive medications that are more or less effective during pregnancy at managing blood pressure? Or even more basically, are the dosages we currently use correct? With such a large study group, we could have learned which medications could be used safely during pregnancy, at what dosages, and with which groups of women. It is likely that some women should absolutely not be given medications due to confounding health conditions.

To answer any of these questions would have been highly useful and added significantly to the body of scientific research on pregnancy hypertension. In its current form, however, this study adds little, if anything, to our understanding of the pregnancy hypertension, the use of medications to control hypertension during pregnancy or their potential negative side effects. All this study tells us is that blood pressure medications tend to lower blood pressure and evoke complications in some women. Well, of course they do. That is not novel. We knew that already.

There are so many missed opportunities here. Not parsing the medication, dosage data was an egregious omission; one that makes me wonder why it was funded and why it was published in such an esteemed journal. And with 15 authors attributed to this study, why did no one on the masthead push to expand the analytics beyond what was presented? Pregnancy hypertension can be deadly and there is a striking lack of research in this area. Why are we not asking the big questions?