Q. Has anyone done any research on how much lactase is needed to balance out 1 gram of lactose?
Trial and error. That's all there is. Just trial and error.
Seriously, the problem is that each individual is different. Most people still manufacture some lactase, even if they are LI, so they only need sufficient additional lactase to balance out what they're missing. And the type of food eaten, how and when it is eaten, and even when the lactase is taken all have effects on what the symptoms might be. There are -- and probably can't be -- even rough approximations given out.
Q. Will taking acidophilus pills help my LI symptoms at all?
The most I can say is, maybe. Here's why:
The symptoms that people associate with lactose intolerance -- gas, bloating, diarrhea -- are actually caused by the bacteria and other microscopic organisms (the flora) in your colon taking the undigested lactose that makes its way past the small intestine (where it should get absorbed) and fermenting it, releasing a lot of gas in the process. Different bacteria like lactose to different extents. Some gobble it up, releasing huge amounts of gas; some ignore it, creating few problems.
Lactobacillus is a genus of bacteria. There are many species of Lactobacillus, some of which are used in the manufacture of yogurt, including (aha) Lactobacillus acidophilus. They have the property of making their own lactase, the enzyme that digests lactose. (That's why yogurt is usually better tolerated by those who are LI than other forms of milk products.) So there is some logic in thinking that increasing the concentration of lactobacillus in one's colon would lessen LI symptoms. The big question is whether taking the pills would actually do that. And I just don't know if that's true.
There has been much more attention paid to the role of colonic bacteria in LI over the past few years, but I don't know of any solid research that has anything to say about whether lactobacillus or acidophilus actually helps, whether it's acting as a placebo, or whether other factors are involved. But it's an area I'm going to watch closely in the future.
Q. Is whey protein a problem for people with lactose intolerance?
Whey itself is the liquid portion of milk that is left over when the casein protein (curds) is removed. This liquid also contains almost all the lactose that is in milk. So when whey protein is manufactured, it depends on the purity of the manufacturing process whether all the lactose is removed.
I have seen on the shelves of natural foods stores several brands of whey protein that label themselves as lactose-free. If you are concerned, you should look for one of these.
Q. What, if any, are the differences between the terms lactose intolerance, lactose maldigester, and lactase deficiency?
You've touched on a sore point. Technically, the three terms mean slightly different things. You are a lactose maldigester if a clinical test indicates that you do not digest all of the lactose you eat or drink, regardless of whether you get any noticeable symptoms or not. You have a lactase deficiency if you do not produce your full potential amount of lactase, no matter what the cause of this might be, and no matter whether you drink milk or not. Since neither of these terms mention symptoms, we should reserve lactose intolerance for those times when having lactose actually causes symptoms.
In practice, of course, everybody outside of a medical journal just talks about lactose intolerance, and uses it to embrace all three definitions. Even in medical journals, doctors tend not to make fine distinctions. They use one term and stick to it. (In European, especially Scandinavian, medical journals, doctors will use hypolactasia in place of any of these three terms. The opposite condition is known as normolactasia.) Don't worry about terminology. Use lactose intolerance. Everybody will know what you mean.
Q. I'm lactose intolerant, but neither of my parents are. If lactose intolerance is inherited, how is this possible?
Some people produce lactase all of their lives. Others find that their lactase production gradually slows or even stops as they grow older. This is controlled by a gene on the second of the 46 pairs of chromosomes that humans have. There are two forms of the gene, one for lactose intolerance, which we can think of as "stop," and one for continued milk drinking, which I'll call "go."
One set of each pair of genes comes from our fathers and one set from our mothers. Therefore, a person's individual pair can be one of only four possibilities: Mother stop with Father stop; Mother go with Father stop; Mother stop with Father go; Mother go with Father go.
The go gene is dominant and the stop gene is recessive. That means that if you have a stop and a go, go always wins. Lactose tolerance is genetically dominant. When you stop to think about it, this has to be true. A mere 10,000 years ago, virtually everybody in the world was lactose intolerant. Today over a billion people are not. For a trait to spread across the world that quickly, it must obviously be dominant, so that it will be transmitted to children even if only one of the parents has it. (Originally the go gene must have appeared through random mutation. If nobody drinks milk as adults, the trait sits there quietly and does nothing. But if adult milk drinking provides even a slight reproductive advantage, as it probably did by providing better nutrition, the trait is likely to spread through that population.)
With this as background, let's go back to your case. Your mother must have had a stop gene paired with a go gene, making her lactose tolerant. The same with your father. You just inherited the one in four chance of getting the stop half from both your parents, giving you a stop paired with a stop, and making you lactose intolerant.
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