In my A & P (anatomy and physiology) class this week, there were several topics we were exploring dealing with bones and the skeletal system. Part of the discussion was around bone health, which of course leads to calcium intake and vitamin D. The discussion transitioned to lactose intolerance. From there, I was curious about induced lactose intolerance because I think I did that to myself years ago. It was the early 90’s, at the height of the fat phobia that took over the country. I bought into it so steered clear of anything at all that had fat in it. Dairy fell into that category for me.
After not consuming dairy [other than in very small amounts periodically] for probably at least a year or so, I had a craving for chocolate milk. I bought non-fat milk [obviously] and some Ovaltine. I was drinking a HUGE glass of the stuff daily for about a week, and every day that week, well let’s just say I realized it must have been the milk that was creating some unpleasant symptoms.
Nowadays I do consume dairy, butter and cheese for example (I’m not a milk drinker) almost daily and I have no adverse reactions to it. Although I know that these foodstuffs have far less lactose in them than milk does. So that just might be the case (that I’m lactose sensitive, not lactose intolerant).
Lactose intolerance, also called lactase deficiency and hypolactasia, is the inability to digest lactose, a sugar found in milk and to a lesser extent milk-derived dairy products, like butter and cheese for example. It is not necessarily a disorder but more of a genetically-determined characteristic.
Lactose intolerant individuals have insufficient levels of lactase. Lactase is an enzyme that catalyzes the hydrolysis of lactose into glucose and galactose in the digestive system. In most cases this causes symptoms which may include abdominal bloating and cramps, flatulence, diarrhea, nausea, borborygmi (rumbling stomach), or vomiting  after consuming large amounts of it. Some studies have produced evidence that milk consumption by lactose intolerant individuals may be a significant cause of inflammatory bowel disease. [2, 3]
Most mammals normally stop producing lactase, becoming lactose intolerant, after weaning,  but some human populations have developed lactase persistence, in which lactase production continues into adulthood.
Here are some interesting statistics:
It is estimated that 75% of adults worldwide show some decrease in lactase activity during adulthood. 
The frequency of decreased lactase activity ranges from 5% in northern Europe through 71% for Sicily to more than 90% in some African and Asian countries.  This distribution is now thought to have been caused by recent natural selection favoring lactase-persistent individuals in cultures in which dairy products are available as a food source. 
While it was first thought that this would mean that populations in Europe, India, Arabia and Africa had high frequencies of lactase persistence because of a particular mutation, it was later shown that lactase persistence is caused by several independently occurring mutations. 
And this is interesting. While searching to find information about self-induced lactose intolerance I came across this…
As noted above, after infants are weaned there is a genetically programmed reduction in lactase synthesis which results in low lactase activity in adults. This is known as lactase non-persistence, and it results in the incomplete digestion of lactose. I found this terminology involved in lactose absorption/intolerance: 
- Lactase non-persistence (or lactase insufficiency) – indicates that brush border lactase activity is only a small fraction of the infantile level, a condition documented by analysis of brush border biopsies. Recently it has been shown that a genotype (C/C) of the lactase promoter gene is responsible for lactase non-persistence, and demonstration of this genotype can be used as indirect evidence of lactase non-persistence.
- Lactose malabsorption (LM) – indicates that a sizable fraction of a dosage of lactose is not absorbed in the small bowel and thus is delivered to the colon. Since such malabsorption is virtually always a result of low levels of lactase, there is a nearly one to one relationship of lactase non-persistence (or deficiency) and LM. LM is objectively demonstrated via measurements of breath H2 or blood glucose concentrations following ingestion of a lactose load.
- Lactose intolerance (LI) – indicates that malabsorbed lactose produces symptoms (diarrhea, abdominal discomfort, flatulence, or bloating). It should be stressed that this symptomatic response to LM is linked to the quantity of lactose malabsorbed (as well as other variables), i.e., ingestion of limited quantities of lactose does not cause recognizable symptoms in lactose malabsorbers, while very large doses commonly induce appreciable LI symptoms. As a result, the prevalence of lactase non-persistence or LM could far exceed the prevalence of LI symptoms in population groups ingesting modest quantities of lactose.
This source notes that a public health problem can result when folks self diagnose for lactose intolerance (and any other condition of course). This is because these folks might be lactase persisters or even lactase non-persisters that may actually have undiagnosed irritable bowel syndrome (IBS) or other intestinal disorders, given that symptoms are similar. 
I find this interesting because I do have digestive issues that I haven’t pinpointed the root cause of. And yes, I’m trying to diagnose myself. It’s part of my charm.
Considering the large quantities of milk did affect my system, that I know for sure based on my consumption of it and the results pretty soon after, and that now things like butter and cheese don’t bother me, I’m going to say that I am somewhere between lactose non-persistent and lactose malabsorption.
My newest diagnoses of my digestive issues are around FODMAPs and nightshades. I find eating these does make my symptoms worse.
FODMAPs are short chain carbohydrates (oligosaccharides), disaccharides, monosaccharides and related alcohols that are poorly absorbed in the small intestine. These include short chain (oligo) saccharide polymers of fructose (fructans) and galactose (galactans), disaccharides (lactose), monosaccharides (fructose), and sugar alcohols (polyols) such as sorbitol, mannitol, xylitol and maltitol.
The term FODMAP is an acronym, deriving from Fermentable, Oligo-, Di-, Mono-saccharides And Polyols. The restriction of these FODMAPs from the diet has been found to have a beneficial effect for sufferers of irritable bowel syndrome and other functional gastrointestinal disorders. [10, 11] FODMAPs that are not absorbed in the small intestine pass into the large intestine, where bacteria ferment them. The results are production of gas, and the resulting bloating and flatulence associated with that gas production.
FODMAP examples include fruits like apples and cherries, grains like wheat and rye, lactose containing foods (we’ve touched on that already), legumes like chickpeas and lentils, artificial sweeteners, vegetables like artichokes and brussel sprouts and avocados. There are many others in each of these categories too.
Nightshades belong to the Solanaceae family which includes over 2,000 species. They also include some of the most popular foods consumed today, and many of my favorites, unfortunately. Examples include tomatoes, potatoes, all types of peppers, and eggplant. The Solanaceae family contains cholinesterase inhibiting glycoalkaloids and steroid alkaloids including, among others, solanine in potato and eggplant, tomatine in tomato, nicotine in tobacco, and capsaicin in garden peppers. The glycoalkaloids in potatoes are known to contribute to IBS and negatively affect intestinal permeability. [12, 13]