A recent study on high protein has been making the media rounds lately, with some news sites using headlines such as “Eating large amounts of meat, cheese may be as deadly as smoking.”
Note: We’re about to get science-heavy. You can scroll to the bottom for the takeaways. We’ve also summarized important points along the way.
The study itself was part epidemiological and part rodent intervention, and can be found here. In assessing the role of IGF-1 in cancer and aging, they took data from a pre-existing survey (NHANES III; one of the largest American-based national surveys of health and nutrition), assessing 6381 adults over the age of 50.
After getting baseline data on protein intake (averaging 16% of caloric intake; 69% of this being animal-based protein), they then divided people into three groups: the highest third (above 20% protein), lowest (below 10% protein), and a middle group (so they could compare the categories).
After dividing everyone into one of these three groups, they looked at the data for these people over the course of the next 18 years to see if mortality or disease in any of the groups differed.
The individual pieces of data they found from dietary analysis were: - A positive correlation between moderate and high protein intakes and diabetes-related mortality, relative to the lowest intake. This persisted, albeit to a lesser degree, when looking at people over the age of 65. - No relation between higher protein intake with all-cause mortality, cancer-related mortality, or cardiovascular mortality overall. A small increase in risk was seen when looking only at people between the ages of 50-65. This risk was reversed for people above the age of 65, where dietary protein had a protective effect against all forms of mortality (excluding diabetes-related).
When investigating IGF-1 levels (this is separate because the sample is now reduced to 2,253) they found:
The controls in place to reach this conclusion were restricting the age to people over the age of 50 only, and after assessing protein intake, they controlled for overall calories and other macronutrient intake as well as the sources of protein (either animal or plant). Further controls mentioned were age, race/ethnicity, education, sex, disease status, smoking, dietary changes, and attempted weight loss.
NHANES III gets its nutritional data via 24-hour dietary recall.
A quick note on epidemiological studies - they take data after-the-fact and try to make connections. This is not the same as a randomized clinical trial. This is a very important distinction to make, as epidemiological information cannot be used to state that “A causes B.” It is meant to spur further research.
The above bits of data are all that was available from the epidemiological evidence. A separate rodent study was then conducted to attempt to verify causation. It found:
There do not appear to be any significant listed conflicts of interest in this study, with the only disclosed affiliation being the corresponding author (one author having equity in L-Nutra; a provider of medical foods). Funding was provided by NIH/NIA which had no role in producing the methodology.
First, it should be mentioned that to fully appreciate this study we must view it as two studies. There is an epidemiological study and there is a mouse intervention study; anytime tumor growth is mentioned, it refers to the mouse study, and causation can only be applied to the mouse study. It cannot be applied to the human study (as it is an epidemiological study).
As such, we’ll address each one independently:
Epidemiology study in humans
This study noted a 2 to 4-fold increase in mortality. This may sound large, but is too small to be directly compared with smoking. That range in smoking has been noted in thorough analysis of studies when referring to overall mortality, yet it is still much less than the 20-fold expected increased risk for lung mortality. Not only do repeated studies on a topic refine and lessen the initial estimates (the first estimates are almost always too high, which are lessened with subsequent meta-analysis), but information on smoking controls biochemical confounds that predict mortality. This study did not. A direct comparison between the two, despite having similar risk ratios, is misleading.
No participant was under the age of 50, and people were divided into either 50-65 or 65+.
Beyond that, there do seem to be interesting results. There was an increased risk of diabetes-related death. This is unique, since the other mortalities and overall mortality were only higher in those between the ages of 50 and 65. For those older than 65, it was reduced. Mortality seemed to be associated with IGF-1 concentrations in all cases, and IGF-1 activity seemed to be negatively associated with the protective effects seen in those over 65.
Higher protein seemed to mean higher mortality between the ages of 50-65. Once over 65, it actually reversed (unless you were diabetic)!
In regards to the data collection and controls, it seems quite adequate. 24-hour dietary recollections from NHANES III are acceptable (self-reported dietary recollection will always be flawed to a degree) and this was supported by serum IGF-1 concentrations. It should also be stated that the sample size was reduced to about a third when it pertains to IGF-1 (due to not having measurements in everyone).
Quite a few unanswered questions
Many good controls were in place, but there are a few questions that readers may have that this study cannot address:
Many questions arise from an epidemiological study, which is common. It is important to remember these that this is a function of how they are run, and thus why they cannot prove causation.
Ultimately though, this study is good evidence to suggest that IGF-1 is not only playing a role in the aging process and mortality, but that it is also tied into overall protein intake, and this initially harmful effect may eventually turn protective in the elderly. It is a good study if you omit the grandiose claim of meat being as harmful as smoking.
Intervention in mice
This study proves causation in mice, and was used indirectly to support the role of IGF-1 in humans. The study was quite interesting in regards to tumor size (a 78% reduction in size from dietary modification is nothing to scoff at), but there are a few things to address before delving into the study:
With that out of the way, this mouse study noted that protein didn’t necessarily have a protective effect (the vast majority of mice, be it on low protein or high protein, experienced tumor implantation and the tumors stayed there) but it suggests an ‘anti-growth’ effect of lower protein intake or, conversely, a pro-growth effect of higher protein intakes. The type of protein did not matter, since soy also augmented tumor growth to a similar degree as casein.
It demonstrated, perhaps via a correlation again, that tumor growth was associated with IGF-1 activity. This makes logical sense. IGF-1 is an anabolic agent to most cells, be they skeletal or tumor cells! While a GH inhibitor was not used, they did use a GH-deficient line which produces less IGF-1 and found significantly less effects of protein on tumor growth suggesting a causal role.
Higher protein means more IGF-1. IGF-1 is an anabolic agent that causes cell-growth, regardless of type. Skeletal tissue (good) or tumor cells (bad), it does not differentiate.
Other considerations for those that want to know more
In regards to dietary protein overall, the general observation of increased mortality has been noted in other epidemiological research in healthy cohorts, although the magnitude of this increased risk is lesser than observed in this study, with a nonsignificant increased risk of 1.02 (95% CI of 0.98-1.07) and elsewhere a conclusion that increasing protein by a decile increased overall mortality risk by 2% (95% CI of -1% to 5%); to clarify, if the CI (confidence interval) crosses the 0 point the data is not seen as statistically significant.
Interestingly, both studies noted that carbohydrates had a protective effect on mortality (specifically cardiovascular mortality), leading to a hypothesis that perhaps increased protein seen in this study is merely a proxy measurement of reduced carbohydrate intake; plausible due to food sources nor carbohydrate intake in the protein groups being measured, but at this time that hypothesis cannot be addressed with the study in question. If true, however, it would pinpoint protein as accidentally being a red herring in the mortality issue.
Finally, nutritional epidemiology such as this is known to have larger effects whenever a study on a new topic (i.e. mortality in otherwise healthy people) is introduced which the magnitude being significantly reduced when subject to future meta-analysis. This refers to the 2 to 4-fold increased risk (hazard ratios) noted in the study though as the 23 to 73-fold risk being compared to smoking was statistically misleading (and noted by the authors as such), and when paired with the previously cited other studies on mortality it should serve to show that the degree of risk suggested by this study may be an overstatement.
In single-study situations, it seems like everything we eat is associated with cancer. One must look at the full body of evidence.
It is always important to look at the full body of evidence, not just one paper. To that end, as the paper showed that high protein was potentially an issue for diabetics, the question to ask is:
Are there any studies done that directly look at diabetics and protein-intake?
high-protein diets are effective in improving various markers of cardiovascular risk in people with diabetes and should be considered in the overall strategy of diabetes management.
This systematic review and meta-analysis showed that interventions with higher protein diets can actually improve glycemic control and cardiovascular risk in diabetics. This doesn’t prove that higher protein diets decrease mortality in diabetics, it does show discordance between epidemiological and intervention studies. It does remind us to keep an eye on the bigger picture.
Should I stop eating meat?
Whether you do or not, it shouldn’t be because of this study. If you eat a lot of heavily smoked and processed meat, it may be a smart choice to eat more slow cooked and non-smoked meat
This study was also done on people over 50 years old. In fact, it found higher protein was beneficial for those older than 65 (unless they had diabetes). Unless you fit that bill, don’t be too concerned.Should I switch to plant based sources of protein?
Not if you don’t want to. Beyond the hype you may have read, the actual data found that they were either equal (in mice) or that was slightly better (epidemiological).
Should I be worried about IGF-1?
IGF-1 causes cell growth. It doesn’t care if it it’s a muscle cell or an organ cell or a cancerous cell. This same scary-sounding hormone is what helps you build more muscle when you lift weights. Eating protein seems to increase IGF-1. If your underlying diet is poor (too much processed meat, not enough exercise), then high protein intake may be an issue.
Yes, dietary protein was implicated in mortality. No, it isn’t as harmful as smoking. The number which the comparison was borne from (diabetes-related mortality) does exist in the study and is immediately followed by:
“We underline that our hazard ratios and conﬁdence intervals may be inﬂated due to our sample size and the extremely low incidence of diabetes mortality in the low protein group. Overall, there were only 21 diabetes deaths among persons without diabetes at baseline, only 1 of which was from the low protein group”
To even suggest that eating protein is as bad as smoking is pure sensationalism.
Human nutrition is a complex topic, and isolating one area can be complicated. Often times, two disparate issues can be combined together incorrectly:
Issue 1: as we explained, IGF-1 is responsible for cell growth, and it does not care what kind of cells it is growing. For those who exercise regularly, IGF-1 is a boon. For those that have poor diet without exercise, it is not.
Issue 2: poor diet is a ubiquitous problem. Processed meats are a staple of poor diets. Processed meats also tend to have protein. The study made no differentiation between different animal sources. As previously stated, chicken breast is not comparable to processed bologna meat.
When you combine Issue 1 and Issue 2 without looking at the bigger picture, one can mistakenly infer that “high protein is bad for you.”
A more accurate headline for this study would have been “High protein for those between 50 years to 65 years old who have poor diet and lifestyle habits may be associated with increased cancer risk.”
Want to know how much protein you should be taking? We looked at the scientific evidence on the recommended intake.
PRL-8-53, a synthetic nootropic compound, has been examined and added to the database. PRL-8-53 is taken for its ability to boost short term memory, though it does not have a lot of evidence for its effects.
PRL-8-53 was created by Nikolaus R. Hansl while he was studying a class of molecules called benzoates. Giving PRL-8-53 to rats showed very promising memory-enhancing effects. In 1978, a human study was conducted. It involved PRL-8-53 supplementation and a subsequent memory test. People that initially scored low on the test benefitted greatly from supplementation, while high performers did not see improvement. PRL-8-53 was compared to nootropics like piracetam, which helps people with poor memory, while having no effect on people with a good memory.
Unfortunately, no additional evidence has been published since that study. Though there is no data to disprove PRL-8-53’s effects, the benefits noted in the lone human study have not been replicated independently.
PRL-8-53 cannot be recommended as a dietary supplement because of the unexplained drop off in research, and because the original studies were funded by the patent holder and have not been replicated.
Today at Examine.com, we bring you a page on Origanum vulgare, also known as oregano.
Oregano is a popular spice and contains an oil component, which can be supplemented for an immune boost.
Research on oregano began in the 1980s. Its potent antioxidant and antibacterial properties lent themselves well to food preservation. Antioxidants are able to prevent the oxidation of fatty acids, which meant oregano could slow down the speed at which meat went bad and fruit browned. The antibacterial properties were also useful, particularly for storing meat.
It was hypothesized that these properties might extend to the human body as well, but there has been little research done on the matter. A single study on people using oil of oregano to ward off an intestinal infection was published in 2000. While the oil appeared to be very effective at eliminating the infection, the study was funded solely by a producer of oregano oil.
Further research is needed to determine if oregano’s effects really do apply to the human body.
The spice Crocus sativus, also known as Saffron, has been added to the Examine.com database. This expensive spice has several surprises up its sleeve, including a set of unique molecules and an ability to combat depression.
Saffron contains a group of molecules called carotenoids that are water soluble, but only in the context of saffron. Normally, carotenoids are fat soluble.
Repeated human trials have concluded that saffron is effective at treating depression, when taken at the standard dose (30mg a day for eight weeks). Its potency is comparable to several prescription drugs.
Research has yet to determine how exactly Saffron achieves this effect. Preliminary evidence suggests it manipulates serotonin signalling, but the exact mechanism has yet to be pinpointed. Prudent supplementation is advised, because saffron can become toxic to the body if used improperly. Doubling the standard dose and time frame (60mg for sixteen weeks) can do damage to the body. Until there is more evidence for saffron’s effects and toxicity, care should be taken during supplementation.
Over the past decade, no supplement has been as recommended as Vitamin D. Unlike its antioxidant cousins, Vitamin C and Vitamin E, vitamin D is something we tend to be deficient in. In fact, many regulatory organizations have started to bump up their recommended daily intake from 400 IU/day to roughly 800 IU/day.
In the past few months, there has been some push back against vitamin D, most notably from The Lancet. They have recently published a plethora of meta-analyses, many of which conclude that vitamin D’s utility is overstated (you can see our analysis of one of their meta-analysis on vitamin D and bone health here). Most of these studies have been interpreted by the media in a very “black or white” manner - either vitamin D is useful, or it is useless.
It should be noted that no compound will be a panacea for everything. Everyone has their own diet, which leads to different deficient vitamins and minerals in the body.
While there are some outlandish associations with vitamin D with weak evidence (an easy one - that vitamin D leads to a testosterone boost), we thought it would be useful to take a step back and look at the big picture.
Vitamin D has been the “hot” supplement for the past decade, which means it inevitably got hyped beyond what it could actually do. We need to stop over-reacting to the latest research, and remember to keep an eye on the big picture.
We have addressed the recent meta-analysis to investigate vitamin D and its interactions with bone mineral density, and recently another meta-analysis which had a more encompassing goal was published investigating the role of vitamin D in vascular (heart and stroke related), skeletal (total fractures), and cancer outcomes. While the title seems interesting (and we’ll delve into it shortly), its conclusions are being circulating in some media sources as evidence that vitamin D “confers no health benefits” or that future trials are “unlikely” to support vitamin D supplementation.
The recent meta-analysis appears to be well conducted. They investigated double blind trials with either vitamin D in isolation or the combination with calcium, eliminated confounds such as dairy-enriched vitamin D products or interventions not given to both vitamin D and placebo groups, and eliminated studies with known comorbidities so they could more directly analyze the endpoints they wanted to (vascular, skeletal, and cancer outcomes). The study was funded by the Health Council of New Zealand which had no role in the design or conducting of the study. The study failed to find any interaction between vitamin D supplementation (usually in the range of 400-800 IU), with or without calcium, on any vascular endpoint (myocardial infarction, ischemic heart disease, cardiovascular disease, cerebrovascular disease, or stroke) or on cancer outcomes. No relationship was found even when controlling for baseline vitamin D status.
When investigating skeletal outcomes with regards to fractures (different from the previous meta-analysis covered), overall there was no significant association between supplementation and outcomes regardless of whether calcium was included or not. When investigating further, there was a benefit for reducing hip fracture in institutionalized patients. Community dwelling adults (those not in clinical settings and more likely to be purchasing vitamin D supplements on their own) did not, however, see a benefit to fractures that was deemed clinically significant. Clinical significance in this study was deemed a reduction in risk of 15% or more.
When looking at overall mortality (usually the ultimate end goal of interest), there was uncertainty in the results. When they assessed whether vitamin D could reduce the risk of death by 5% or more, the overall applicable sample size was only 60% of what was deemed statistically optimal; a proper statistical conclusion on mortality, due to this, could not be reached and it was deemed of uncertain status.
The latest The Lancet meta-analysis looked at vitamin D supplementation in the context of vascular, skeletal, and cancer situations.
This recent meta-analysis seemed well conducted and should not be disregarded. The relevant takeaways:
Cardiovascular disease is really not something vitamin D is catered to help treat or solve, and the failure of vitamin D having any benefits is no surprise. While aiming for a 15% reduction in risk may seem like the inefficacy of vitamin D was forced, it was chosen so that the magnitude was large enough to have practical benefits in the real world. Due to statistical reasons and subpar ‘ideal’ sample sizes, whether or not vitamin D reduces mortality by more than 5% cannot be answered with this study.
While a perfect study is pretty much impossible to conduct (hence why the body of evidence is greater than any one study), this one was pretty good. The discussion section does mention what evidence would be required to overturn the results which is always a good discussion to hear, and the reasoning that studies requiring over 50,000 people in sample size to yield a positive result have led to some articles stating that future articles are ‘unlikely to support vitamin D supplementation’ (shortsighted - it should be specifically mentioned for the studied parameters; vascular, skeletal, and cancer outcomes).
That being said, conclusions such as ‘no health effects’ are still much too grand to be associated to this study. This study could not assess everything, and claims that can still be made about vitamin D and its benefits include things such as colorectal cancer risk (this meta-analysis covered all cancer outcomes), multiple sclerosis, actual muscular control in the elderly (although the lack of reduction in fractures could argue against this), mood changes with regards to seasonal affective disorders, and diabetes risk. Some issues, such as the increase in testosterone and overall mortality risk, are still in a grey area.
The study was well-done, but to go from “had no effects on general vascular, skeletal, and cancer health” to “has no health effects” is a stretch (to say the least). It should also be emphasized that it looked at general cases, not specific cases.
As we previously cautioned, one must look at the entire body of evidence, not just at the latest research. With that in mind, if you look at our Vitamin D page (more specifically, at our Human Effect Matrix), you will find a plethora of evidence that shows areas that vitamin D has a proven positive effect on. These include:
The original RDI of vitamin D, ~400 IU/day, was actually the minimum you need to not get rickets. The above benefits usually come from higher levels of vitamin D in the body, which can be usually obtained with roughly 2000 IU/day. If measuring the blood concentrations of vitamin D, usually you want to be either in the adequate range (50-75nM or 20-30ng/mL) or slightly higher. You do not want to be insufficient (25-50nM or 10-20ng/mL) or outright deficient (less than 25nM or 10ng/mL).
Vitamin D supplementation has a host of positive benefits. One must consider both the full body of research and also look past the quantitative (how long you live) and consider the qualitative (how well you live).
Overall, vitamin D is both cheap (roughly 5 cents for a daily dosage of 2000 IU) and safe (is not toxic except at absurdly high levels). While it may not fix everything, it has enough benefits to warrant taking.
Vitamin D is cheap, safe, effective, and most people are in a deficient state. If you do not get enough direct sunlight exposure, supplementation is the prudent choice.
Today at Examine.com, we bring you a page on Chromium, an essential mineral implicated in regulating glucose metabolism and insulin.
Chromium is found in plants, specifically grains. It is part of a protein called chromodulin. Chromodulin is responsible for the actions of insulin receptors, and it increases in activity as more chromium ions bind to it.
Supplementation of chromium should be examined through the frame of deficiency. A subclinical deficiency is when the body has lower than normal levels of chromium, but not to the point of a true deficiency. A true deficiency is characterized by inactive chromodulin. Supplementation of chromium is very beneficial during a true deficiency, but it is often touted as useful during a subclinical deficiency as well.
However, if there is no deficiency state, the evidence does not support chromium’s ability to enhance glucose metabolism in the body. Some researchers have observed benefits for insulin sensitivity, glucose, body weight and quality of life in diabetic people, but these effects are very unreliable, both in terms of frequency and magnitude.
Chromium supplementation may also be able to reduce carbohydrate cravings and binge eating patterns, but more research is needed to confirm these effects.
A recently published Lancet article about vitamin D and bone mineral density is making waves in the medical world and on the web. It calls into question whether Vitamin D should be recommended to all community-dwelling adults for osteoporosis prevention.
This meta-analysis sought to investigate the interactions between vitamin D supplementation and bone mineral density (BMD). BMD is a proxy measurement for fracture risk that, while not always accurate, is usually a good indicator of fracture risk. Changing your lifestyle can have an impact on your BMD within the year, whereas to measure risk directly would require much larger sampler sizes and numerous years of tracking.
While bone mineral density (BMD) is not a direct measurement of fracture risk, it is a solid and measurable indicator.
The authors argued that previous meta-analyses on vitamin D and fractures were of low quality due to the available data being of limited statistical power, inappropriate doses, or not in deficient populations.
A new meta-analysis questions whether blanket vitamin D recommendations are suitable for osteoporosis prevention.
The meta-analysis assessed 19 studies on Vitamin D supplementation which analyzes bone mineral density. The studies invested were studies using vitamin D supplementation of either D2 or D3 form in adults. Age was not limited to older people, and if calcium was taken with Vitamin D then the placebo group must have also received calcium. Thus, some of the studies are just vitamin D, while others are vitamin D + calcium vs placebo + calcium.
The inclusion criteria were a bit vague, and this may have been to broaden the search (and thus include more data). That being said, while permissive inclusion criteria can include more data, they can also add so much data that benefits to one group of people (e.g. the elderly, women, etc.) can be lost because people in other groups are included. For these complications, we look further in the data to when factors are controlled for.
Inclusion criteria are the characteristics of the subjects in the study. Having both young and elderly in this meta-analysis could have influenced the results.
At the outset of the study, the meta-analysis found that at the four areas of the body where bone mineral density was measured, only one (femoral neck) saw a small benefit with supplementation. The other four (hip/trochanter, lumbar, forearm, and total) did not; the confidence intervals (CI values) all crossed the zero point, indicating no statistical benefit.
The authors concluded the study prior to doing any analysis of the cohorts in their data, and as such we cannot use this data to conclude anything about the age groups.
At the outset, a major complication with this study would be how it had a very large and permissive inclusion criteria set to allow many studies to be analyzed yet it did not do further analysis into whether there were commonalities in the studies that showed benefit versus those that don't. The question "did including younger adults cause an apparent benefit in elderly people to be missed" cannot be answered without further statistical analysis. It should be noted that six of the included studies (comprising 871 subjects, about 21% of the total subjects analyzed) had a mean age under 50. This could have influenced the results if we assume the elderly would benefit more from Vitamin D supplementation than youth (which, according to the previous literature, is a very sound hypothesis).
Furthermore, vitamin D levels in serum were quite variable, as at baseline in these studies there seems to be quite a mix of studies with baseline Vitamin D below 30nM (five studies), between 30-50nM (three studies), 50-75nM (eleven studies) and one above 75nM. When looking at Vitamin D concentrations in serum after supplementation, it remains a variable 53-92nM (the range of the averages across the studies).
Penultimately, while perhaps of lesser importance due to standardization in the past suggesting intramuscular and oral supplementation of the following doses are somewhat bioequivalent, there was still a large variability in studies giving daily (thirteen) or weekly/monthly (four) oral supplementation and injections once a year (two studies).
Finally, while the studies in the subject were 92% women, which may simply be something that should be mentioned in the reporting of this study as the actions of vitamin D on bone health are somewhat comparable between men and women (although perhaps a bit more robust in women due to usually more advanced and common osteoporotic symptoms than men).
Overall, there are very limited practical conclusions we can draw from this study.
To start, remember that we need to keep an eye on the prize. While bone mineral density (BMD) is a useful measurement for bone fractures, the ultimate issue we are concerned with is injuries and death from falling, especially in the elderly. Vitamin D supplementation has been shown studies to decrease falls and fractures in the elderly. That's important!
Various studies show that in the elderly, vitamin D supplementation decreases falls and fractures.
The broad inclusion criteria means that in general, we can say that Vitamin D does not help improve BMD. As vitamin D is not generally recommended to alleviate osteoporosis in the general population, it would have been beneficial for the analysis to include a breakdown for a variety of age groups.
The bottom line is that we care most about preventing fractures and subsequent death. The people most at-risk for those are the elderly, and several studies show that vitamin D helps prevent such falls. The Lancet study focused on the entire adult population.
When you factor in the prevalence of vitamin D deficiency, the myriad of other health benefits of vitamin D, its low cost, and how safe it is, it is our opinion that vitamin D supplementation is a safe and intelligent choice.
This past year has been huge for Examine.com. We did a lot of research. Our team grew. Our traffic grew. And we started to enter the mainstream consciousness.
While our goal from day one was to bring some clarity to supplementation, we never thought we would be as successful as we've been. Every day, roughly 17,500 people visit Examine.com to learn more about supplementation and nutrition!
At the same time, we know we can be better. Much better. We need to be more accessible. We need to balance theoretical with practical. We need to make Examine.com "mom friendly." Average Joe and Jane are overwhelmed by our information, and thus still easily swayed by marketing hype.
With that in mind, we are extremely excited to announce that Dr. Spencer Nadolsky is the new Director of Examine.com (aka, the man-in-charge). A medical doctor (who lifts!), he'll be balancing the research side with the application side. A no-nonsense and pragmatic approach to supplementation and nutrition.
As a company, we're all about focusing on what we're best at. Dr. Nadolsky is the best man to lead our future growth while our research team continues to bring you the most reliable, neutral, and independent information on supplementation and nutrition.
With your support, we're confident 2014 is going to be a big year for Examine.com.
It is a brand new year with exciting things to come from Examine.com. With our new editors working harder than ever, we just hit over 27,500 references on the site! Continue to keep your eyes open for continual editing and up to date changes on your favorite supplements.
New evidence has come to light about the effects of a popular tea and herb: valerian (Valeriana officinalis). We’ve updated our page on the supplement because new evidence suggests valerian has no significant effect on sleep.
When first studied, valerian was thought to have positive effects on sleep, which led to it being marketed as a natural sedative herb. Researchers postulated that valerian was able to enhance the signalling of a major sedative neurotransmitter, called gamma-aminobutyric acid (GABA), to bring about its effects. Further human studies have found no quantifiable benefit to sleep. This means that despite many people reporting that they had a better night’s sleep after supplementing valerian, scientists were unable to observe any specific improvements, like a reduction in how long it took someone to fall asleep or how an increase in their total time spent asleep.
Though valerian may enhance GABAergic signalling, it also degrades into two molecules that actively compete with the sedative effects of this signalling. This may be the reason why initial research was so promising, but follow-up studies failed to find any benefits to sleep.
Valerian shows promise in relieving anxiety, but the evidence at this time is not strong enough to recommend it over other options. Further study is also needed to determine if valerian has a positive effect on sleep quality.