23 Comments
founding

Exactly what I needed this week. My dental patients are now asking me about what medications they should be taking because they are questioning the MDs who always push another pill. Not knowing much about the anti-hypertensives, this was a phenomenally times post and will help me to help others. Thank you!!

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Your patients are so lucky to have you as a dentist! I loved what you said in our interview about being a quarterback for your patients' health. It's a good thing that so many people no longer blindly trust doctors, but most still need some guidance to help them make decisions that benefit their health.

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Yup, I have spoken with Goldhamer and with one of their staff doctors, and I can already see that it's drifting lower with my monthly 3-day fasts, so I am pretty optimistic that with a longer fast, I might establish a lower plateau.

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The BP thing is still a mystery to me. I went down significantly on a #WFPB diet years ago, but since then the climb somewhat resumed. My hope now is that I will be able to do a course of supervised fasting at TrueNorth in California, and break through what seems to be a plateau on the way down...

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Fasting is spectacular for lowering BP.

Did you eat a high salt diet in your younger years? It seems that sodium intake in early life may set people up for rising BP in midlife and beyond, even if they drop their salt consumption.

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That is interesting about the high salt intake. I would say yes. Until I went full #WFPB in 2015, I was certainly not moderating salt, and eating lots of cheese and salty snacks. I now do 3-day water fasts at home once a month and try do do intermittent fasting as a routine. I really want to go for a supervised fast for a week or 10 days, I thing that will help me restore completely normal BP without meds.

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There's a very good chance that it will, based on Goldhamer's published studies.

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That’s interesting too and sad.

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author

Yes, it is rather sad. By the time people wake up to the fact that what they put in their mouths has a huge effect on their health and function, they may have already done some serious damage. Fortunately in most cases that damage is reversible, if the person is willing to make radical changes to the way they live. It's only a small minority who will do that though, in my experience.

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Feb 10Liked by Robyn Chuter

Does BP gradually naturally worsen as people age , all things people equal ? eg would the BP of a 75 yo kalahari bushman be worse than their 25 yo BP ?

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author

Great question, which was answered by the INTERSALT study. In a nutshell (an unsalted one, mind you), populations that are not exposed to salt beyond that which naturally occurs in their diets, do NOT experience an age-related increase in blood pressure. In fact, people eating a traditional African diet based on tubers, maize and vegetables, hit their highest blood pressure in their early to mid-20s and then their blood pressure slowly declined as they aged.

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WOW !

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Here's one of the publications from INTERSALT: https://www.bmj.com/content/312/7041/1249. They measured urinary sodium excretion as it's a much more accurate marker of sodium consumption than people's self-reported sodium intake (coz people lie about what they eat!). "Higher urinary sodium is also associated with substantially greater differences in blood pressure in middle age compared with young adulthood."

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What a comprehensive reply. I respect the time it took to put it together, and I'm attempting for short replies in response to each study.

I have read each of these studies you cited. It took awhile. I listened and carefully considered before replying. Here's somewhat of only an initial comparison of what your data is competing with.

The previously posted vid was by a Dr. to Dr's/healthcare conference. Tiny history excerpt.

--First known case of heart attack in the US, 1912. became the leading cause of death, 1930.

--Cancer 1811 0.5% death. 1900 5.8% death, 2010 31.1% of deaths.

--Type 2 DM 1900 Rare, 1935 0.37%, 1960 0.91%, 2015 9.4% of population.

The reason I recommend this vid, is because it offers a historical comparison that is hard to ignore when tiny fractional gains are discussed..

It just so happened that YT, posted an updated vid of his talk in my feed after reading your studies over the past week. The data is more comprehensive and now has been updated with a linear regression model for sugar as a variable of low significance. P=.0001 I think. You can watch this vid 35 mins at 1.5x speed to save time. In fact it would be better to watch the vid than read my notes which took 6-8hrs of reading and more time to compose a response to.

https://www.youtube.com/watch?v=PvZk-jNqzgE

my comment. What we are currently told to believe is, that animal meat or products after all history became lethal in 1912 at least in the US and the biggest cause for health troubles. It really improbable, that meat which 'turned apes cognitively into men' suddenly is killing men.

The vid speaks historically about different groups of people who went from eating different types of diet before taking on the standard American diet. It does cover both vegetarian carb and essential a carnivore type of diet.

I don't know what are the whole causes, and I think there are many modern 'innovations' which contribute that are not seed oils. high fructose corn syrup might be another, in combination. I'm sure there are likely others. My choice was to revert to a food type that was more like Pre industrial revolution type of foods which didn't appear to cause trouble just 120 years ago.

So now to your studies.

The first study. https://pubmed.ncbi.nlm.nih.gov/27434027/

I have a different take on this study, but because of it's method, weak data improved by large numbers, maybe the data is substantial enough to say something.

A meta analysis study Among 6,124 abstracts, 102 trials, including 239 diet arms and 4,220 adults,

with a 5% change carb to fat. What is the other 95% of the diet, what was displaced!

SFA no change in fasting glucose.

MUFA slight change in fasting glucose, lower insulin

PUFA significant change in fasting glucose, ~10x change than Mufa, lower insulin

They are appearing to call it an improvement that insulin must drop farther to maintain a fast.

Two ways this could be taken. They didn't test insulin without fasting. So it's kinda useless.

At least in the fasting sense, this strongly appears to me that they are LESS insulin sensitive.

What if a person feels more hungry the lower their insulin goes. What happens? Do the feel more compelled to eat?

What if the lower insulin means it's harder to lose weight while you feel worse?

Replace all carbs with PUFA, how low will the insulin need to go to survive a fast and maintain ketones/sugar?

Is this suggesting eating fried anything in PUFA oil foods, swapping butter for margarine and lard for Crisco.

Does it improve health, I see no outcomes?

--

https://pubmed.ncbi.nlm.nih.gov/24550191/

Overfeeding study. Why is overfeeding, with anything, or a seed oil mixed with a carb good? Targeted weight gain?

Why not compare a historical eaten good animal food if you want to compare SFA to PUFA?

This compares fructose plus SFA or fructose plus PUFA looking for what.

Results, you can make your IR go up with either, but you might look better eating PUFA?

I'm not sure how to pull better health info out of this.

Does it improve health?

--

Third study. PUFA's lower blood pressure study. by a difference of ~0.4mmg

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6668335/

They also found that US individuals consumed the most PUFA, and had a BMI of 5 more than everyone else.

I'm also kind of surprised they found so many individuals to test with normal BP.

What is the health improvement of a person with Normal BP to have it lowered by 0.5mmg VS a BMI of 5 higher?

--

Fourth study. Comparing one PUFA against what? It is not comparing it with animal proteins or SFA. If so teach me.

In the paper's history, it cited worsened health with PUFA as a reason to do this study.

https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.118.038908?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%252520%2525200pubmed

I didn't see any info related to insulin resistance. This is not a small miss!

There's a lot of variables in there, I'm not going to look into it. So if it reduces risk by 20%, relative to what?

--

Fifth study. Because Genetics might increase PUFA, your healthier?

https://pubmed.ncbi.nlm.nih.gov/33924952/

I only saw the abstract. Who can change their parents? This might sound trite, where is this going, changing one's DNA?

--

6th study. Goal. To assess the effect of reducing saturated fat. replacing it with whatever anyone wants.

Another study of studies.

Results,

"56 people need to reduce their saturated fat intake for ~four years for one person to avoid experiencing a CVD event"

BUT NO CHANGE IN MORTALITY. This seems really strange!

At least this is comparing SFA against something. They are not even saying what source SFA is.

----

So now I have reviewed all of the data you have cited to support something that approximates your method for good health. This seems more like managed decline with no real recovery, just slightly minimized risk. Just not appealing to me.

I have previously studied keto as a treatment somewhat at length, not just YT testimonials, studies. Even people who do it poorly seem to have some success. Lately, 'carnivores' are seeing faster results, I suspect, partly because some modern veg combined with IR irritates some more than others(insert pesticides, gmo plus other stuff as possible)

Here is my N=1.

I switched to keto years ago, well reduced PUFA too. I lost weight to a point. However. BS was more responsive at 2hrs. BP down, HR down.

At holiday times, I've eaten pufa plus carbs with family on some days. Seem to gain 10# each year. notably higher bp, hr, and bs.

Interested in recovering, maybe losing a little more, fasted, short and longer time periods, monitored BS during fasts and time to low BS and transitions to fasted state. Drops to baseline BS faster, which I think is lower stored sugar, faster switching to gluconeogenesis. While my bs was normal, it rested on the high end of normal and recovery was normal but not fast. Fasting improved responsiveness and gradual overall lower bs. Holiday food reverses this improvement.

I'm a lot less hungry, and eat less, although, mostly eggs or healthy meat now. Total calorie intake is way down.

Eat 4-5 eggs, 240-300 calories, last's a lot longer than a single 500 cal PUFA muffin. This carries me till 2-5pm eat a small meat meal. Might have a piece of no gluten bread when I wake, and piece of no sugar cacao at some point. Fairly boring and stable. This goes up when I physically labor.

I'm a lot healthier than all my similarly aged peers. I'm not likely to switch back. Rather, I should do more fasting, as it helps the most. Presumably, to correct for my intake of food in times past.

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With all due respect, I don't think you understand the methodology of any of the studies you've attempted to criticise. For example, you don't seem to grasp what HOMA is actually capturing, nor what a substitution analysis involves, nor how and why researchers select outcomes to study (hint: measuring hard outcomes such as death or heart attack requires huge populations and long follow-up periods, and the vast majority of grant funding does not allow for this).

I'm happy to continue this conversation if there is any value in it, but I'm not going to waste my time on attempting to have a scientific discussion with someone who is merely looking to invalidate any arguments for a contrary point of view, based on his/her personal experience.

Let me know if you are actually interested in a detailed response to each of your criticisms of the studies, and if so, I shall invest some time in doing so.

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What I've read is that there is a very high corollary between elevated insulin and increased blood pressure. Prediabetes, high insulin wo necessarily high blood sugar, as insulin keeps blood sugar in check (storing fats) but does so much more. Reports list 90% are pre diabetic now, cases of fatty liver disease on the rise as well as non alcoholic FLD are on the rise and in children also. One doesn't have to look overweight to have high insulin levels. Reportedly, stateside, this isn't checked unless you are likely in the latter stages of Diabetes. I met with high resistance just to have a check.

Often the lowering of the BP goes concurrently with lowering glycemic index and load, lowering the need for insulin. I can confirm this experientially.

How to change, many argue about which diet. Developing information is pointing strongly towards polyunsaturated fats being incorporated into ones own fat stores, which are acting as a hormone increasing insulin resistance. It's not necessarily high glycemic foods fault, however, you won't lose polyunsaturated fat eating carbs or polyunsaturated fats.

I've lost weight eating keto, but found a better response to predominantly beef/lamb/chicken/salmon and eggs, without shying away from physical work, but no extra working out, which would probably help. Almost endless vids on the subject. In fact anyone reading substack I would presume has already searched this out. Just in case. Here's a starter video on the history of...

https://www.youtube.com/watch?v=7kGnfXXIKZM

Many have eliminated the need for bp meds by going on these food choice modification.

Done cheaply? You should choose your Dr. after being as informed as possible.

my experience. Delay breakfast eat as many Eggs to make you full, meal 2, grass fed ground beef. Cream in coffee ok. Maybe better if switch to decaf. Low carb veg stuff is expensive to fill up on, and contains dramatically less nutrition per dollar. 5 eggs a day, plus 1lb grass fed 70/30 ground meat 1.50$+4-5$.

Cow's fat is dependent on the cow's diet, grass fed beef fat has significantly lower polyunsaturated fat. This has been well documented.

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author

I'm in total agreement that hypertension is linked with insulin resistance; this is the metabolic syndrome. However, my clinical experience and my reading of the scientific literature leads me to give very different dietary advice. To make this a valuable exercise for all my readers - and for me too - please provide the scientific references that support your dietary recommendations, and I'll critique them and provide mine.

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I'm uncertain where to start, the subject is so broad, interested in tightening the scope of question. The vid above does take a little while, but if unfamiliar with the info, it would take me far longer to type it. I'm interested to have a discussion, hope I have enough depth to be interesting, as I see it as the greatest chronic health crisis that effects likely more than 95% of the population. Solving it early would eliminate most sick care jobs.

I will add a little reference which might seem unrelated, but be patient. Also note, I want to find more studies, but lately AI helping search engines is especially unfriendly as well as papers citing recommendations rather than testing results..

A cow's fat makeup, glance down the column for differences between pufa vs saturated, and mono vs saturated.

https://www.sciencedirect.com/science/article/pii/S0309174013004944

You might consider these cows adolescent to early mid life. They are harvested just after they've reached their peak feed conversion to total body weight ratio. (not as fully aged adults such as use who've been eating a lot longer)

Why cow fat? I haven't ever seen study on humans fat makeup which compares a confined diet to body fat make up. (see vid) Humans have diet history, and sudden diet changes don't change fat makeup composition. Grains have higher density nutrition and PUFA's. The composition of the cows fat changes rapidly with unsaturated fat gaining much more quickly. Grain fed cows hit their peak harvest weight 5-6 months younger weighing 200lbs more than their grass fed counterparts. (nafld?) Consider, they are vegetarian afaik, albeit the twin stomach type, they are not lying when they fill out the questionnaire while hanging on the meat hook. (most pufa's come from seed oils)

N=1. Writing from my view looking inward.

Weight loss or PUFA loss? Math. Krebs cycle fat -> ATP. There is only so much energy needed in a day, and it's usually less the older you grow. Fully saturated fat converts easily, polyunsaturated fat has several to many many double bonds to solve through many extra chemical steps, process to get to ATP. It costs more energy to make it that way and takes longer, it also requires Antioxidants (not sure what bears do in the winter) in the correct quantity to balance they equation, onsite ready to go. Or no conversion. The body tends to convert the easiest fuel and stores the rest if it has to(insulin).

If i want to lose weight and PUFA ergo, I must minimize useless calorie processing.

Meat has a glycemic index of 0. It's nutrient dense. What is the lowest PUFA meat then, or most heathy meat? if different. Some use the Omega 6:3 ratio, 6 is more likely to have follow on unsaturates. from memory bc search engine not helping.

Wild caught $almon 1:1, lamb 1:1, Grass fed beef 3:1, Grain fed beef 6:1, Chicken 11:1, Pork over 30:1. Not shaming the pig, consider what they are fed.

Cholesterol. Is this a concern about a primarily meat diet? if so say on.

My highest cholesterol was found when I had fasted 3 days to check my insulin level while fasting. The doc was visibly shaken by the numbers, higher than she had ever seen. Why. Low insulin, fat and all other cells release it to be converted to ketones and to a little sugar because the body has to have it to live. You only have about 4 tsp of sugar in your whole bloodstream, if your body didn't have sugar, without cholesterol conversion to backfill as sugar stores waned, well, it wouldn't take long. What would my cholesterol have looked like if I spiked my insulin? Selah.

For anyone new to this and have more time, consider looking through the titles on yt, under low carb down under and so many other places.

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I'm really not interested in watching videos of people who don't cite studies in humans to support their contentions.

I'm no fan of adding any type of oil to one's diet, but there's just no evidence that omega 6-rich oils have uniquely deleterious effects on human health. For example:

1. This study - 'Effects of Saturated Fat, Polyunsaturated Fat, Monounsaturated Fat, and Carbohydrate on Glucose-Insulin Homeostasis: A Systematic Review and Meta-analysis of Randomised Controlled Feeding Trials' (https://pubmed.ncbi.nlm.nih.gov/27434027/) - found that "Replacing SFA [saturated fatty acids] with PUFA [polyunsaturated fatty acids] significantly lowered glucose, HbA1c, C-peptide, and HOMA." That is, when humans were given 'seed oils' in place of saturated fat, they became more insulin-sensitive and their carbohydrate metabolism improved.

2. This study - 'Overfeeding polyunsaturated and saturated fat causes distinct effects on liver and visceral fat accumulation in humans' (https://pubmed.ncbi.nlm.nih.gov/24550191/) - deliberately overfed 39 young, normal-weight individuals muffins high in SFAs (palm oil) or n-6 PUFAs (sunflower oil) for 7 weeks. "Both groups gained similar weight. SFAs, however, markedly increased liver fat compared with PUFAs and caused a twofold larger increase in VAT [visceral adipose tissue] than PUFAs. Conversely, PUFAs caused a nearly threefold larger increase in lean tissue than SFAs. Increase in liver fat directly correlated with changes in plasma SFAs and inversely with PUFAs. Genes involved in regulating energy dissipation, insulin resistance, body composition, and fat-cell differentiation in SAT [abdominal subcutaneous adipose tissue] were differentially regulated between diets, and associated with increased PUFAs in SAT. In conclusion, overeating SFAs promotes hepatic and visceral fat storage, whereas excess energy from PUFAs may instead promote lean tissue in healthy humans." In other words, overeating saturated fat causes an increase in visceral fat while overeating omega 6 fat has the reverse effect.

3. This study - 'Effects of n-6 PUFAs compared with SFAs on liver fat, lipoproteins, and inflammation in abdominal obesity: a randomized controlled trial' (https://pubmed.ncbi.nlm.nih.gov/22492369/) - "randomly assigned 67 abdominally obese subjects (15% had type 2 diabetes) to a 10-wk isocaloric diet high in vegetable n-6 PUFA (PUFA diet) or SFA mainly from butter (SFA diet), without altering the macronutrient intake." Body weight increased by the same amount in both groups, but liver fat was lower during the PUFA diet than during the SFA diet. The inflammation markers TNF receptor-2 and IL-1 receptor antagonist were lower on the PUFA diet, while insulin levels were higher on the SFA diet. "Compared with SFA intake, n-6 PUFAs reduce liver fat and modestly improve metabolic status, without weight loss. A high n-6 PUFA intake does not cause any signs of inflammation or oxidative stress."

4. This study - 'Relationship of Dietary Linoleic Acid to Blood Pressure' (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6668335/) - found that higher linoleic acid intake was associated with lower systolic and diastolic blood pressure.

5. This study - 'Biomarkers of Dietary Omega-6 Fatty Acids and Incident Cardiovascular Disease and Mortality: An Individual-Level Pooled Analysis of 30 Cohort Studies' (https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.118.038908?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%2520%25200pubmed) - found that "Higher levels of LA [linoleic acid - an omega 6 fatty acid] were significantly associated with lower risks of total CVD, cardiovascular mortality, and ischemic stroke, with hazard ratios per interquintile range of 0.93 (95% CI, 0.88–0.99), 0.78 (0.70–0.85), and 0.88 (0.79–0.98), respectively, and nonsignificantly with lower coronary heart disease risk (0.94; 0.88–1.00)." In other words, high blood levels of the principal fatty acid found in seed oils was associated with a lower risk of heart disease and stroke.

6. This study - 'Causal Effects of Serum Levels of n-3 or n-6 Polyunsaturated Fatty Acids on Coronary Artery Disease: Mendelian Randomization Study' (https://pubmed.ncbi.nlm.nih.gov/33924952/) - found that people who genetically express higher levels of linoleic acid in their blood have a lower risk of coronary artery disease.

7. This Cochrane review - 'Reduction in saturated fat intake for cardiovascular disease' (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8092457/) - found that "cutting down on saturated fat led to a 17% reduction in the risk of cardiovascular disease (including heart disease and strokes), but had little effect on the risk of dying. The review found that health benefits arose from replacing saturated fats with polyunsaturated fat or starchy foods. The greater the decrease in saturated fat, and the more serum total cholesterol is reduced, the greater the protection from cardiovascular events. People who are currently healthy appear to benefit as much as those at increased risk of heart disease or stroke (people with high blood pressure, high serum cholesterol or diabetes, for example), and people who have already had heart disease or stroke. There was no difference in effect between men and women."

I could go on (and on, and on....) but hopefully I've made my point. The arguments made by those who claim that seed oils are the cause of all modern maladies do not pan out when one looks at studies conducted on human beings. I reiterate that I don't think anyone should be adding vegetable oils to their diet, but that is because most people are overweight, and oils displace foods of higher nutritional value.

While it is true that saturated fatty acids yield more ATP than polyunsaturated fatty acids when oxidised, it is also the case that PUFAs are preferentially oxidised because they are more reactive. This results in a higher tendency of the body to store SFAs (especially in visceral fat depots), as demonstrated in study #2 cited above.

As to why your cholesterol level when up after a fast, all fasting practitioners know that this happens as a consequence of mobilisation of energy reserves. Cholesterol cannot be converted to ketone bodies; it's triglycerides that are broken down into fatty acids and glycerol, with fatty acids subsequently being converted into acetyl CoA and then ketone bodies. (See https://bio.libretexts.org/Courses/Lumen_Learning/Anatomy_and_Physiology_II_(Lumen)/10%3A_Module_8-_Metabolism_and_Nutrition/10.04%3A_Lipid_Metabolism.)

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Thank you for watching. I started reading, this will need time for me to read.

This took time. After some reading and thought, will consider what I learn.

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I tried to answer not trivially, but with fewest words, the hurdles to the studies not being useful to the discussion of SFA from grass fed meat, or PUFA from something else.

My whole goal in reply in scope to your concern that my meat diet may not be healthy.

I offer this with as much data in the shortest time of any easy listening vid I recall.

Paul Mason, MD compares and differing lipids and their deadly effects in Atherosclerosis using many studies with dramatic differences. It's 26 mins. Would, a 62% increase in rate of death. There's also particular risk to women also, study n=48,000, starting at 26% risk in prior heart trouble up to 61% with seed oil. Watch the whole vid to hear the details and the parameter data.

https://www.youtube.com/watch?v=XFFT4C1OcPY

If you are unwilling to review the data provided, you will be missing what you would need to teach me of a safer way.

Through some pain, I learned to listen with more humility to whom I didn't think i'd learn from for hidden treasure. Blessings.

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author

I decided to watch this video after all. My commentary is at https://robynchuter.substack.com/p/diving-down-the-low-carb-rabbit-hole.

By the way, the criticisms that you made of the studies that I cited had nothing to do with saturated fats from grass fed meat.

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author

I don't watch videos, I read studies. If you want to engage in serious discussion of scientific matters, provide me with the scientific citations, or just stop wasting my time.

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