Category: Food

Month 50: caffeine #50to50

I drink too much caffeine. In college, I was notorious for drinking multiple cans of coke a day. In grad school, I made the switch to Diet and lost 10 pounds in a month. That was my peak Chipotle phase, too, clocking in around 175.

In the past few years, since moving to California, I’ve drastically reduced my caffeine intake from Coke (having made the switch to Coke Zero, which my crude palette likes as much if not better than original Coke, and miles better than Diet). I basically order it when we eat out, which is a few times a month, and on weekends once in a while. I estimate that I currently drink 5-10 cans a month.

However, I inhale coffee. I have at least two (large) cups in the morning (one on waking up either at home or at Starbucks, another on reaching work) and another in the afternoon (usually to stave off hunger from intermittent fasting). I also will make a cup in the evening if I need to stay up, and on weekends I typically have a few cups too. I estimate that I drink about 75 cups of coffee a month.

I can’t give up on coffee. I’m not really an aficionado of the taste – I can tell great coffee from terrible, but good vs bad coffee is not always clear. Low standards indeed, because for me it is purely functional. I did go nuts over Pumpkin Spice for a while but I’m well and truly over that now. My go-to drink at Starbucks is a flat white with sugar free hazelnut and vanilla, just enough flavor to keep me interested but not attentive. The bottom line is, I don’t get enough sleep, so I drink coffee.

However, caffeine after 2:00 pm has long been shown to interfere with sleep:

  • Caffeine consumed 0, 3, and 6 hours before bedtime significantly reduced total sleep time. Even caffeine consumed 6 hours before bed reduced total nightly sleep amounts by more than 1 hour.
  • Caffeine consumed at all three points diminished sleep quality. Caffeine taken 3 and 6 hours before bedtime, as well as caffeine consumed at bedtime, significantly increased the amount of time spent awake during the night.
  • Disruptions to sleep as a result of caffeine were perceived by volunteers (as recorded in sleep diaries) for caffeine consumed at bedtime and 3 hours before bed, but were not reported for caffeine taken 6 hours before bed. However, sleep monitors measuring total sleep time and sleep efficiency (time spent sleeping relative to total time spent in bed) showed that caffeine consumed 6 hours before bedtime had significant detrimental effects to both.

That third point is the most surprising. It means that even if you don’t perceive an impact on your sleep, there still may be one. I haven’t tried to replicate the study on myself because I don’t have/want a sleep tracker, but the point is compelling.

(Here’s a full-text link to the actual study)

This makes it easy to resolve to stop drinking caffeine after 2pm and limit myself to two cups of coffee a day. I’ll just switch to water (which I drink a lot more of since buying myself a cool hydroflask with a Joshua Tree design).

Table 3 from the study referred to above. Click for full-text link.

Replicated food is not halal or kosher: a secular argument

Fake meat is going mainstream – you can buy burgers at Burger King, White Castle, and Del Taco. Surely Chipotle and McDonalds are not far behind. This is exciting for people like me who are Muslim Eaters obsessed with the halal scene. But plant-based meat is one thing, what about the science fiction dream of totally replicated meat?

The basic concept of the replicator in Star Trek (and now, The Orville) is that food is just molecules, so instead of cooking plants and animals, you can assemble the dish (and the dish upon which it is served) from raw molecules of matter. Which then leads to the inevitable question, would replicated pork be halal or kosher?

Rather than make a theological argument for why it would or would not be, I want to approach that question from the other direction. Why would it be? The basic answer is that the molecules from which we replicate the pork don’t actually come from a pig. They could come from stockpiles of carbon, nitrogen, hydrogen, and oxygen (CHON). There probably would be some trace molecules too, but if the replicator can assemble foods by molecule, then it can probably assemble molecules from atoms. These are just implementation details. Therefore, if the meat doesn’t come from a pig, then there’s no problem. Of course there are additional requirements of halal and kosher with regards to how the animal is slaughtered, etc. But we by removing the animal from the equation, these requirements are moot.

The problem is that the molecules of pigs don’t originate in pigs, either, Ultimately, molecules are formed from atoms, and atoms are formed mostly from cosmological forces (all the good stuff in particular from supernovae). So, consider two groups of molecules. Both are formed from the same supernova explosion of a star that was birthed from primordial hydrogen in the Big Bang. One group of molecules never enters the biosphere and gets processed into raw stock, and then replicated into a pork chop. The other group of molecules ends up in a pig, and then excised into a pork chop. One of these is clearly not halal or kosher. However, the origin of the molecules is identical. It’s purely a matter of how these molecules were arranged since they were created, that renders them non halal/kosher. IN another billion years, both will end up part of the same gas cloud in an expanding red giant anyway, and that brief arrangement into “pig” will just be a tiny blip.

What if you then collected those molecules from the second group, the group that was for an insignificant period of time, a pig, retrieved them from the gas cloud, and then reassembled them into a porkchop? (This is the nonsensical kind of thing that I imagine bored superintelligent post-singularity entities would do for self-amusement, which is so ludicrous but inevitable that it is another reason why I am skeptical of the singularity and AI in general). This reconstituted porkchop is still not halal or kosher.

Think about that. Out of 20 billion years, a negligible period of time being arranged into a pig renders these molecules forever, inescapably, non-halal and non-kosher. There is something profound and eternal about form, about morphology, that transcends time and space.

I don’t pretend to understand my faith rationally. It’s faith, after all. But the above thought experiment says to me that there is something more to halal and kosher, than merely about the animal. There is something inherently impure in the morphology itself. By recreating the morphology, we are in a sense recreating that impurity. So, the only safe answer, is no. Replicated pork is not halal or kosher. Replicate turkey bacon instead.

UPDATE: As a friend pointed out, wild boars do die and decompose, so their molecules can be re-purified if they end up as grass eaten by a cow that is slaughtered according to halal/kosher. So there must be some kind of re-purification process that can undo the impurity of the brief morphological state. So, by analogy, the replicated food in a replicator can be halal/kosher even if the molecules were briefly non-halal/non-kosher. as long as they were “laundered” through the biosphere first. Still, assembling the molecules into a porkchop would still return to the forbidden morphology, so the answer to the main question is still no.

UPDATE 2: In the comments below, J. sends this link discussing in detail whether cloned pigs are kosher. (spoiler: they aren’t). However, the discussion therein still leaves the door wide open for replicated pork. I still hypothesize no.

Pizza and Pie: Chicago vs. New York (vs. Chicago)

When people ask what’s “better” – New York pizza or Chicago Deep Dish, it is important to clarify whether they really mean Deep Dish, or whether they actually mean stuffed pizza (or pizza pie, as I call it).

Before anyone can begin to compare deep dish to NY style, they need to understand what deep dish actually is. Deep dish, as represented by Uno’s, Gino’s East, and (the best) Lou Malnati’s, is thick flaky crust, sliced mozzarella cheese, toppings, crushed tomato sauce. Pizza Pie, however, fails the definition of being pizza because it is actually thin crust, shredded mozzarella cheese and toppings, a second thin crust, and then sauce. This is why it is more of a pie or a casserole than a pizza, at places like Giordano’s or Connie’s.

With these clarifications in place, we can evaluate the differences between true deep dish and NY style. The infographic below is courtesy of Lou Malnati’s and is a fair comparison. As you can see, NY style is thin crust, sauce, cheese, toppings.

When I make pizza at home, I do it in an iron skillet, but I actually make a Pequod’s inspired pizza, which is a kind of hybrid: thick crust, sauce, toppings, sliced cheese. this is because I lack the skill to make the true crushed tomato sauce necessary to protect the cheese, and I like the carmelized crust effect from layering mozz over the edges on contact with the pan. Here’s the last one I made:

hybrid deep dish - Aziz P style
hybrid deep dish – Aziz P style

And now, the actual infographic. Are you not entertained?

Infographic-Chicago-vs-New-York-Pizza

Related: RealDeepDish.com’s exegesis of the styles of Chicago pizza.

is nothing sacred? scaremongering about Ramen noodles at TED

This video is as misleading as it is disgusting:

The basic premise is that they had someone swallow a small pill containing a tiny camera, and filmed the digestion process for instant ramen noodles, gatorade and gummy bears versus more “natural” versions of those foods. And shocker, the processed foods did not seem to digest as quickly as the non-processed versions. There’s also some chemical scaremongering about how the ingredients in Ramen are “related” to butane which is a component of gasoline.

The whole thing is clumsy and ham-handed and (of course) gross; basically, the recipe for instant viral success. But just because the noodles retain their shape longer hardly means they are not being digested; if they were really immune to acid then they’d come out in the same shape as they went in (a rather obvious point ignored by the artists here, who have clevely titled their project M2A for “mouth 2 anus”)

The top-rated comments on the video also are worth sharing as solid critiques:

62+ packets assuming the maximum allowed amount of TBHQ (0.02% per product). I’d worry more about sodium intake before then (and ramen is full of sodium, natural or otherwise, no arguing there).

Oh, then this gem– “survive Armageddon”– ramen has an official shelf life of about 6 months. It’s flash-fried and then quickly dried. This is the major preservative. TBHQ preserves the oils.
But what do I know? I don’t have a fancy degree in media art production like Ms Bardin.

This video is just misinformation and half-truths. “Artificial flavours are intellectual property”? True, but they are disclosed to the FDA (in the US). The FDA must approve all artificial colours and flavours. No ifs or buts.
TBHQ is chemically related to butane, in so much that it contains a butyl moiety. So does butter. Butter and butane share a root word– butyrum. Butter is natural. Where’s that info in this video? Plus, you’d need 62+ packets @ 80g to get 1g of TBHQ, the “sick” amount.

fear Japan, part 3,343: the poop burger

look, you really don’t need to click this link, because you basically have already figured out what lies at the other end. This is far, far worse than the synthetic poop machine, or nuclear poo, or walls of poop. This is a poop burger. I mean, why bother clicking? Just know that the link exists, it’s real, and that it’s Japan. That’s basically enough.

You can’t imagine how much it pains me to assign this post to the Food category. Given how many posts on this blog involve the topic, I am surprised I haven’t created a poop tag before now, though.

unchi!

diet, cholesterol, and heart disease skepticism?

I’m involved in a debate over diet and health over at Dean’s and in the course of that debate, was encouraged to read a paper by Corr et al. that suggests low-fat diets are essentially useless for reducing heart disease. This post started out as a comment but it grew enough to warrant a post in it’s own right. So, let’s look at what the Corr paper is actually saying, shall we?

The international bodies which developed the current recommendations based them on the best available evidence[1-3]. Numerous epidemiological surveys confirmed beyond doubt the seminal observation of Keys in the Seven Countries Study of a positive correlation between intake of dietary fat and the prevalence of coronary heart disease[4] although recently a cohort study of more than 43,000 men followed for 6 years has shown that this is not independent of fiber intake[5] or risk factors. The prevalence of coronary heart disease has been shown to be correlated with the level of serum total and low density lipoprotein cholesterol (LDL) as well as inversely with high density lipoprotein.

So, high intake of dietary fat indeed has a positive correlation for coronary heart disease. Corr is conceding this at the very start!

Further, coronary heart disease is also indeed associated with high LDL and low HDL. So far I am not seeing any Cholesterol Conspiracy here… the ADA seems to be right on the ball.

So, we’ve already established that CHD is associated with high fat, high LDL, and low HDL. So, what’s left to argue about?

As a consequence of these studies, it was assumed that the reverse would hold true: reduction in dietary total and especially saturated fat would lead to a fall in serum cholesterol and a reduction in the incidence of coronary heart disease. The evidence from clinical trials does not support this hypothesis.

Hmm. Two sentences here. one about a reasonable inference from the conceded association between fat and LDL with CHD. But ok, let’s call the question of whether teh reverse is true, Question A – “does reducing fat and LDL in the diet reduce CHD?”

And then another sentence, about evidence from clinical trials not supporting that inference. What about those clinical trials, exactly?

It can be argued that it is virtually impossible to design and conduct an adequate dietary trial. The alteration of any one component of a diet will lead to alterations in others and often to further changes in lifestyle so it is extremely difficult to determine which, if any, of these produce an effect. Dietary trials cannot generally be blinded and changes in the diet of the ‘control’ population are frequently seen: they may be so marked as to render the study irrevocably flawed. It is also recognized that adherence to dietary advice over many years by large population samples, as for most people in real life, is poor and that the stricter the diet, the worse the compliance.

Ah. so the available evidence from clinical trials is fundamentally suspect to systematic error. Fair enough. So, any conclusions we make from them should be tempered with that, right?

(long analysis of clinical trials in literature follows)

The message from these trials is that dietary advice to reduce saturated fat and cholesterol intake, even combined with intervention to reduce other risk factors, appears to be relatively ineffective for the primary prevention of coronary heart disease and has not been shown to reduce mortality.

OK, so the trials focusing on low-fat diets alone didn’t show any primary prevention benefit. Well, see caveat above, right? (and Corr’s noted exception about the MRFIT study…)

However, what about secondary prevention?

well, good! But still, is there some reason that maybe we aren’t seeing better results here? Is diet necessary, or sufficient? Let’s look at studies that not only remove fat, but also add HDL:

The first successful dietary study to show reduction in overall mortality in patients with coronary heart disease was the DART study reported in 1989[20]. The three-way design of this ‘open’ trial compared a low saturated fat diet plus increased polyunsaturated fats, similar to the trials above, with a diet including at least two portions of fatty fish or fish oil supplements per week, and a high cereal fibre diet. No benefit in death or reinfarctions was seen in the low fat or the high fibre groups. In the group given fish advise there was a significant reduction in coronary heart disease deaths and overall mortality was reduced by about 29% after 2 years, although there was a non-significant increase in myocardial infarction rates. The reduction in saturated fats in the fish advice group was less than in the low fat diet group and there was no significant change in their serum cholesterol.

Finally, the more recent Lyon trial[21] used a Mediterranean-type of diet with a modest reduction in total and saturated fat, a decrease in polyunsaturated fat and an increase in omega-3 fatty acids from vegetables and fish. As in the DART study there was little change in cholesterol or body weight, but the trial was stopped early following a 70% reduction in myocardial infarction, coronary mortality and total mortality after 2 years.

In other words, adding HDL to your diet helps a lot, whereas reducing polyunsaturated fat (or just increasing fiber) still doesn’t seem to do anything. We’ve established that a modest increase in HDL can help. But have we established that a modest reduction in LDL will not help?

Unfortunately, the design and conduct of these trials are insufficient to permit conclusions about which polyunsaturates and other elements of these diets are the most beneficial. The long term effects of these trials[20,21] and the compliance with the dietary regimes remain to be seen.

So, we don’t really know if these studies answer that question. It’s possible that lowering LDL has a longer-timescale benefit than increasing HDL. These studies don’t answer the question either way, because of the limitations Corr concedes – certainly we haven’t proven that lowered LDL is not genuinely helpful yet.

Anyway, how much LDL was really reduced anyway?

An important aspect of the lipid-lowering dietary trials is that on average they were only able to achieve about a 10% reduction in total cholesterol. The results of recent drug trials have demonstrated that there is a linear relation between the extent of the cholesterol, or LDL, reduction and the decrease in coronary heart disease mortality and morbidity, and a significant effect seen only when these lipids are lowered by more than 25%[23].

Ahhhh. Corr goes on to quote a bunch of studies that show frankly awesome improvements in mortality using drugs to lower LDL by 25% or more.

(in other words, definitively proving that lower LDL does indeed reduce heart disease. We just answered Question A from above).

So, let’s summarize:

conceded by Corr at the outset:
– increased HDL reduces CHD.
– increased fat increases CHD.
– increased LDL increases CHD.

dietary trials:
– somewhat lowered LDL does not reduce CHD.

drug trials:
– significantly reduced LDL does reduce CHD.

caveats:
– dietary trials have systematic errors.
– long-term trials on reducing LDL have not been performed.

special note: The MRFIT trial follow up focused on reducing LDL diet alone, and did show reduced myocardial infarctions over a longer term.

My conclusion from this would be that a. increase HDL now for immediate benefit, and b. reduce fat and LDL in my diet for long term benefit. Seems obvious enough, and fully in accord with what the ADA recommends.

Corr’s conclusion?

diets focused exclusively on reduction of saturated fats and cholesterol are relatively ineffective for secondary prevention and should be abandoned.

umm.. what?!?!

This is where they cross over into vaccines-autism and flouridated water territory, frankly.

What would have made the Corr paper immeasurably stronger would have been for them to devise an experiment that would answer these questions and fill the gaps. That’s always my challenge to these self-styled “skeptics” of the scientific consensus. What’s the experiment you propose? What would you do to make your case?

That’s how science works. Theory drives experiment, experiment refines theory, and back again. If your claim is that available evidence (in this case, clinical trials) don’t support the contention, that’s not enough. You need to come up with an experiment that actually refutes the contention. Formulate your hypothesis and test it! Anything else is just nitpicking from the sidelines, which is how most of these agenda-driven meta-analyses end up reading.

Frankly, I am very much eager to be able to dispense with the low-fat, low-cholesterol crap. Here’s why in a nutshell.

So please, Dr Corr and anyone other “cholesterol skeptics” out there. Show me the proposal for your experiment, and I guarantee you the fast food industry will show you the money.

Coffeegasm: protection against Alzheimer’s

The following has essentially zero impact on my habits, but it is worth crowing about all the same:

A U.S. study has found drinking five cups a day not only protects against Alzheimer’s disease but may even reverse damage.

Scientists at the University of Florida tested the theory on 55 mice bred to develop symptoms of Alzheimer’s, giving half the test group caffeine in their water once signs of memory impairment became apparent.

Astonishingly, and to the delight of the cafe latte set, those dosed up on caffeine performed far better on memory tests and thought-related skills than those who were not given caffeine.

“The results are particularly exciting in that a reversal of pre-existing memory impairment is more difficult to achieve,” said study leader Dr. Gary Arendash in a BBC report. “They provide evidence that caffeine could be a viable ‘treatment’ for established Alzheimer’s disease [sufferers] and not simply a protective strategy.”

“That’s important because caffeine is a safe drug for most people,” he added, “it easily enters the brain, and it appears to directly affect the disease process.”
The team believes the application of caffeine has a preventative effect on the production of both the enzymes needed to produce beta amyloid — the protein which forms destructive clumps in the brains of dementia patients.

Those mice lucky enough to be dosed on caffeine showed up to a 50 percent reduction in the damaging protein. Dr. Arendash has called for further tests to see if the results can be replicated on humans.

So, in a sense I can rationalize my Starbucks habit as a preventive health care expense. Incidentally, this is not the first study to suggest coffee’s beneficial effects wrt AD. Here’s a couple papers on PubMed I found when searching for “coffee alzheimer” – the second one is the paper referred to above.

Alzheimer’s disease and coffee: a quantitative review.
Barranco Quintana JL, Allam MF, Serrano Del Castillo A, Fernández-Crehuet Navajas R.
Neurol Res. 2007 Jan;29(1):91-5.

Caffeine protects Alzheimer’s mice against cognitive impairment and reduces brain beta-amyloid production.
Arendash GW, Schleif W, Rezai-Zadeh K, Jackson EK, Zacharia LC, Cracchiolo JR, Shippy D, Tan J.
Neuroscience. 2006 Nov 3;142(4):941-52. Epub 2006 Aug 28.