whats better ? i use flax seed oild in my casein protein shake befor bed but i found putting flax seeds in the shake make it tast less like s h i t any benifits of useing oil?
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whats better ? i use flax seed oild in my casein protein shake befor bed but i found putting flax seeds in the shake make it tast less like s h i t any benifits of useing oil?
I like the oil in salads. It has a nutty flavor to it. I also use the ground flax seed mixed with oatmeal in the morning. Trader Joe's has em both, but PuritansPride has the lowest price on the oil...
make sure you get the ground up seeds. some people bodies cant break them down.Quote:
Originally Posted by mike954;39***72
i like the seeds for better flavor and the fiber they add.
Flax seeds are a better bet IMO. The seeds, once ground, have a considerable amount of fibre and can be used for their anti-estrogen effects.
Fish oil is the better choice of dietary oils any day of the week.
Both are good. Flax seeds give you the xtra fiber as a bonus, the oil gives a more concentrated o m e g a 3,6 & 9 source of fats...Without the fishy smell that can leach out through your skin pores giving you that fish smell...
I like the oil, you have to eat WAY too many seeds to get enough noticable EFA's.
The prevailing dogma on this site is that flax oil is THE choice dietary oil to supplement.
By no means am I saying flax oil is not a good choice- it is a very good choice for ***** 3s. However, the best choice is fish oil.
I've copied and pasted a post I made a couple months back with respect to this.
If you are choosing between which two oils to supplement your diet with, the choice is, unquestionably, fish oil.
The particular ***** 3 fatty acids found in fish oil- EPA (eicosaphentaenoic acid) and DHA (docosahexaenoic acid)- promote cardiovascular health through helping to optimize cholesterol, reduce chances of sudden death owing to heart conditiong, they have been shown to reduce inflamation, improve joint function, held with ADHD, promote healthy brain function, aid in reduction in bf...the list goes on (a search of PubMed or google will give you a boat load of excellent studies all preaching the benefits of fish oil.
If you are worried about mercury (I agree people worry too much about this), you should purchase a high quality fish oil from small, cold water fish (natural factors, Carlson, etc.)
Although flax oil, which contains ALA, is an excellent source of ***** 3 polyunsat's, the ability of the body to convert flax oil and ALA to EPA/DHA is not good enough to warrant choosing flax over fish oil.
Here are comment, by Lyle McDonald, on recent study with respect to flax & fish oil:
Plourde M, Cunnane SC. Extremely limited synthesis of long chain polyunsaturates in adults: implications for their dietary essentiality and use as supplements. Appl Physiol Nutr Metab. 2007 Aug;32(4):619-34.
There is considerable interest in the potential impact of several polyunsaturated fatty acids (PUFAs) in mitigating the significant morbidity and mortality caused by degenerative diseases of the cardiovascular system and brain. Despite this interest, confusion surrounds the extent of conversion in humans of the parent PUFA, linoleic acid or alpha-linolenic acid (ALA), to their respective long-chain PUFA products. As a result, there is uncertainty about the potential benefits of ALA versus eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA). Some of the confusion arises because although mammals have the necessary enzymes to make the long-chain PUFA from the parent PUFA, in vivo studies in humans show that asymptotically equal to 5% of ALA is converted to EPA and <0.5% of ALA is converted to DHA. Because the capacity of this pathway is very low in healthy, nonvegetarian humans, even large amounts of dietary ALA have a negligible effect on plasma DHA, an effect paralleled in the *****6 PUFA by a negligible effect of dietary linoleic acid on plasma arachidonic acid. Despite this inefficient conversion, there are potential roles in human health for ALA and EPA that could be independent of their metabolism to DHA through the desaturation - chain elongation pathway.
My comments: So I had originally planned to look at a paper on BMR and Spontaneous Ph in response to varying combinations of diet and exercise but, after last issue's massive feature article, I'm not sure it would have added much.
Also, a question I received regarding a statement I made in the updated Rapid Fat Loss handbook about flax oil no longer being an appropriate essential fatty acid (EFA) source, along with some general confusion on various Internet forums about the topic made me choose this week's paper. I'm going to skip what I think is some unnecessary detail and complexity since I don't think it adds to the practicalities of the question I want to address.
By way of introduction, early nutrition research was very concerned with determining what were the essential nutrients for human health and survival. By definition, an essential nutrient is one that is
a. Required by the body for survival
b. Can't be made by the body
It's a bit more complicated than that and there are some nutrients which are defined as conditionally essential (glutamine is one) but this covers the basics.
Vitamins and minerals are essential, about half of the amino acids are essential and, as early research fought to determine, it turns out that some fatty acids are essential. These are called, generally, the EFAs and, as we now know there are two of them.
Due to methodological issues that I won't detail, determining what fatty acids were actually essential was actually a fairly difficult problem in the early part of the 20th century. In early research, it was thought that there were three EFAs, alpha-linoleic acid (ALA, not to be confused with alpha-lipoic acid, an insulin sensitizer), linolenic acid (LA), and arachidonic acid (AA). When it was found that rats could make AA out of LA, it was dropped, leaving two EFAs. I'd note that, at one point, it was thought that LA was the only EFA but, as we now know, both ALA and LA are essential fatty acids.
These two fatty acids are also often referred to by their chemical names (which have to do with their structure) which are *****-3 (n-3,w-3) for ALA and *****-6 (n-6, w-6) for LA.
Now, both LA and ALA are metabolized in the body (this includes a variety of processes including oxidation in the liver) to other compounds, I'll spare everyone the biochemical details.
LA is metabolized to gamma-linoleic acid and then eventually to arachidonic acid. As mentioned above, this is why AA was removed from the list of EFAs; since the body can synthesize it from LA, it's not essential.
ALA is metabolized to EPA (you don't want to know the full name) which is further metabolized to DHA (same comment). EPA and DHA are more commonly referred to as the fish oils since they are found in high amounts in fatty fish.
Now, for the most part, I'm not going to talk much about the LA->AA pathway. The reason is that excess LA/AA is actually detrimental to the body. AA has inflammatory characteristics and excess LA (esp. in relation to ALA intake) is thought to be a harmful to the body. I'd note that studies show that the current ratio of LA:ALA is around 25:1. It's thought that a ratio of 4:1 or lower would be better.
Bottom line, most of us get way too much LA in the first place, unless you eat essentially a zero fat diet you get most of what you need, there's no real need to make lots of AA from a health or survival standpoint.
Of more concern is the EPA/DHA issue which is what I want to discuss in more detail. Both are critical for things like optimal health, fat burning, etc. It looks like DHA may be even more important. Babies accumulate DHA in their brains and babies who either don't receive sufficient DHA (from the diet) or have a rare genetic syndrome can end up with brain damage. DHA is present in large amounts in cellular membranes. Basically, sufficient DHA intake is critical.
Which brings us to the real topic of this week's paper: Can the body convert ALA to EPA/DHA in sufficient amounts? Because, if it can, then using a source of ALA such as flaxseed oil is sufficient. If it can't, then intake of preformed EPA/DHA via fish oils is going to be required.
Now it's clear that the human body possesses the enzymatic machinery to convert ALA to EPA/DHA. But there is an issue of whether the conversion process can occur in sufficient amounts.
Without going into the ridiculous detail of this week's paper, the short-answer is basically "No, it can't." Now, there are some methodological issues with the studies having to do with the amount (giving large amounts of ALA can cause an underestimation of true conversion) given and some other stuff but the bulk of the data points to the simple conclusion that the human body is simply terrible at converting ALA to EPA/DHA.
In fact, studies using flax oil supplementation show no change in DHA levels. None. It will raise EPA a bit but the conversion to DHA is essentially zero.
There are two odd exceptions to the above that I want to mention. The first is in vegans. Due to zero intake of animal foods, they have zero intake of DHA. But while they show lower levels of DHA, they don't show deficiency symptoms. While more research needs to be done, presumably pathways of conversion/production of DHA are up-regulated under this situation.
The other is in extreme w-3 deficiency, where plasma DHA levels typically rise after ALA supplementation. This is just a classic feedback loop, and occurs for other nutrients as well (for example, absorption of certain minerals will increase the more deficient someone is). This probably explains why a lot of bodybuilders (eating nearly zero fat) did get something out of flaxseed oil during the 90's, in a massive deficiency, they got better conversion. Once that deficiency is fixed, conversion rates drop into the toilet.
But beyond that, the overall impact of ALA supplementation plasma levels of EPA is small, for DHA essentially nil. And given the critical importance of both EPA/DHA on human health, fat loss and performance, the bottom line is that this makes ALA (via flaxseed oil or what have you) an insufficient replacement for preformed fish oils.
As a couple of final comments, I'd also note that supplementation of EPA doesn't raise DHA levels either. Since all commercial fish oils I've ever seen contain both EPA/DHA, this is a fairly non-issue. But it is yet another reason why ALA by itself is insufficient. Not only is the conversion of ALA to EPA small, the conversion of EPA to DHA is simply nil, hence ALA won't impact on the body's DHA levels.
Having established that ALA intake is ineffective at increasing EPA/DHA levels, a final and related question to address is whether ALA has any effects above and beyond what EPA/DHA are doing. This week's paper mentions one possibility which is a mild impact of ALA supplementation on cardiovascular disease. It also notes that EPA/DHA supplementation has a greater effect. Other researchers (not all agree) feel that the true EFAs are EPA/DHA, and that ALA is simply a parent compound that is not essential in its own right. Currently I tend to agree with this stance.
Summing up: the body requires EPA/DHA for optimal function. This includes fat loss, prevention of a lot of diseases, controlling inflammation, etc. While the body has the machinery to convert alpha-linolenic acid (ALA, found in high quantities in flaxseed oil), the amount of that conversion is small for conversion to EPA and negligible for DHA. Hence I don't feel that ALA/flax oil is an appropriate EFA source. You need to be taking preformed EPA/DHA (in either capsule or liquid form). This was one of the changes I made to the second edition of the Rapid Fat Loss handbook (the first edition allowed for flax to substitute for fish oil).
Krill Oil
Good call, bro.Quote:
Originally Posted by xlxBigSexyxlx
Although given the cost I always feel like I'm getting more bang for my buck by going with a high quality fish oil (Carlsons is my go-to), which is comparable to most flax oil
Damn fine avy, btw. Has the face of a broad I use to see but, unfortunately, not the hammers :/\: